oxalates and Kidney-Calculi

Oxalate is a divalent organic anion that affects many biological and commercial processes. It is derived from plant sources, such as spinach, rhubarb, tea, cacao, nuts, and beans, and therefore is commonly found in raw or processed food products. Oxalate can also be made endogenously by humans and other mammals as a byproduct of hepatic enzymatic reactions. It is theorized that plants use oxalate to store calcium and protect against herbivory. Clinically, oxalate is best known to be a major component of kidney stones, which commonly contain calcium oxalate crystals. Oxalate can induce an inflammatory response that decreases the immune system's ability to remove renal crystals. When formulated with platinum as oxaliplatin (an anticancer drug), oxalate has been proposed to cause neurotoxicity and nerve pain. There are many sectors of industry that are hampered by oxalate, and others that depend on it. For example, calcium oxalate is troublesome in the pulp industry and the alumina industry as it deposits on machinery. On the other hand, oxalate is a common active component of rust removal and cleaning products. Due to its ubiquity, there is interest in developing efficient methods to quantify oxalate. Over the past four decades, many diverse methods have been reported. These approaches include electrochemical detection, liquid chromatography or gas chromatography coupled with mass spectrometry, enzymatic degradation of oxalate with oxalate oxidase and detection of hydrogen peroxide produced, and indicator displacement-based methods employing fluorescent or UV light-absorbing compounds. Enhancements in sensitivity have been reported for both electrochemical and mass-spectrometry-based methods as recently as this year. Indicator-based methods have realized a surge in interest that continues to date. The diversity of these approaches, in terms of instrumentation, sample preparation, and sensitivity, has made it clear that no single method will work best for every purpose. This review describes the strengths and limitations of each method, and may serve as a reference for investigators to decide which approach is most suitable for their work.

Topics: Animals; Calcium Oxalate; Gas Chromatography-Mass Spectrometry; Humans; Kidney; Kidney Calculi; Mammals; Oxalates

Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis and/or chronic kidney disease. There are different diseases related to hyperoxaluria: (1) kidney stones, 50% of them being explained by intermittent hyperoxaluria, secondary to dietary mistakes such as low hydration, excess of oxalate consumption and/or low calcium consumption; (2) primary hyperoxaluria, a genetic orphan disease inducing a massive production of oxalate by the liver, leading to increased plasma oxalate increase and saturation, and further systemic oxalosis with oxalate deposition, nephrocalcinosis and ultimately kidney failure, the management of this disease being currently dramatically modified by the onset of new therapeutic tools such as RNA interference; and (3) enteric hyperoxaluria, resulting from increased intestinal oxalate absorption because of intestinal malabsorption (short bowel syndrome, bariatric surgery, exocrine pancreatic insufficiency, etc.). Diagnosis and therapeutic management of these diseases require a full understanding of oxalate physiology that we detail in this review.. L’hyperoxalurie, définie par une élévation de l’oxalate urinaire, favorise la survenue d’une maladie lithiasique, d’une néphrocalcinose et/ou d’une insuffisance rénale chronique. L’hyperoxalurie peut témoigner de différentes maladies : (1) l’hyperoxalurie diététique, responsable de 50 % de la maladie lithiasique par le biais d’erreurs alimentaires (hydratation insuffisante, consommation excessive d’oxalate et/ou consommation insuffisante de calcium) ; (2) les hyperoxaluries primaires, maladies génétiques orphelines responsables d’une production massive d’oxalate aboutissant à des dépôts tissulaires précoces (dès l’enfance) et sévères (à l’origine d’une insuffisance rénale terminale puis d’une thésaurismose avec atteinte multiviscérale) et dont le pronostic est aujourd’hui transformé par les nouvelles thérapies (ARN interférents) ; (3) l’hyperoxalurie entérique, résultant d’une augmentation de l’absorption digestive de l’oxalate dans une situation de malabsorption (syndrome du grêle court, chirurgie bariatrique, insuffisance pancréatique exocrine, etc.). La physiologie de l’oxalate, détaillée dans cet article, permet d’appréhender la prise en charge diagnostique et thérapeutique de ces maladies.

Topics: Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Nephrocalcinosis; Oxalates

Kidney stone disease (KSD) is one of the earliest medical diseases known, but the mechanism of its formation and metabolic changes remain unclear. The formation of kidney stones is a extensive and complicated process, which is regulated by metabolic changes in various substances. In this manuscript, we summarized the progress of research on metabolic changes in kidney stone disease and discuss the valuable role of some new potential targets. We reviewed the influence of metabolism of some common substances on stone formation, such as the regulation of oxalate, the release of reactive oxygen species (ROS), macrophage polarization, the levels of hormones, and the alternation of other substances. New insights into changes in substance metabolism changes in kidney stone disease, as well as emerging research techniques, will provide new directions in the treatment of stones. Reviewing the great progress that has been made in this field will help to improve the understanding by urologists, nephrologists, and health care providers of the metabolic changes in kidney stone disease, and contribute to explore new metabolic targets for clinical therapy.

Topics: Humans; Kidney Calculi; Oxalates; Reactive Oxygen Species

Kidney stone disease is caused by supersaturation of urine with certain metabolites and minerals. The urine composition of stone formers has been measured to prevent stone recurrence, specifically calcium, uric acid, oxalate, ammonia, citrate. However, these minerals and metabolites have proven to be unreliable in predicting stone recurrence. Metabolomics using high throughput technologies in well defined patient cohorts can identify metabolites that may provide insight into the pathogenesis of stones as well as offer possibilities in therapeutics.. Techniques including 1H-NMR, and liquid chromatography paired with tandem mass spectroscopy have identified multiple possible metabolites involved in stone formation. Compared to formers of calcium oxalate stones, healthy controls had higher levels of hippuric acid as well as metabolites involved in caffeine metabolism. Both the gut and urine microbiome may contribute to the altered metabolome of stone formers.. Although metabolomics has offered several potential metabolites that may be protective against or promote stone formation, the mechanisms behind these metabolomic profiles and their clinical significance requires further investigation.

Topics: Calcium; Calcium Oxalate; Humans; Kidney Calculi; Metabolomics; Oxalates

Kidney stone is a highly recurrent disease in the urinary tract system. Most kidney stones are calcium stones, usually consisting of either calcium oxalate or calcium phosphate. Supersaturation of soluble calcium, oxalate, phosphate, and citrate in the urine is the basis for calcium stone formation. Genetics, diet, low physical activity, and individual habits contribute to the formation of kidney stones. In this review, the associations of the risk of kidney stones with oxalate consumption and some individual habits, such as smoking, alcohol drinking, and opium consumption, are summarized.

Topics: Calcium; Calcium Oxalate; Habits; Humans; Kidney Calculi; Oxalates

Hyperoxaluria is a clinically relevant metabolic entity that portends a high morbidity burden. Primarily manifesting as kidney stone disease and chronic kidney disease, advanced hyperoxaluria can also affect major organs, including the brain, heart, liver, bone, and the skin. It is categorized based on etiology into primary and secondary hyperoxaluria. Pathology is attributed to excess de novo oxalate production in the former and multifactorial exogenous oxalate absorption or excess intake of its precursors in the latter. Diagnosis often involves demonstrating elevated urinary oxalate levels, especially in patients with normal kidney function. Here in this review, we will perform an in-depth discussion of various causes of hyperoxaluria and describe treatment options. In view of the significant morbidity burden associated with hyperoxaluria, patients could benefit from heightened clinician awareness to aid in the timely diagnosis and management of this condition.

Topics: Humans; Hyperoxaluria; Kidney Calculi; Oxalates

Primary hyperoxaluria type 1 (PH1) is a rare genetic disorder that causes hepatic overproduction of oxalate and, often, nephrocalcinosis, nephrolithiasis, chronic kidney disease, and kidney failure. The purpose of the review is to provide an update on current emerging therapies for the treatment of PH1.. Use of ribonucleic acid interference (RNAi) therapeutics that target the liver to block production of key enzymes along pathways that generate oxalate is a promising approach. Available evidence supports the efficacy of both Lumasiran (targeting glycolate oxidase) and Nedosiran (targeting hepatic lactate dehydrogenase (LDHa)) to reduce urinary oxalate excretion in PH1. The efficacy of alternative approaches including stiripentol (an anticonvulsant drug that also targets LDHa), lanthanum (a potential gastrointestinal oxalate binder), and Oxalobacter formigenes (a bacterium that can degrade oxalate within the gastrointestinal tract and may also increase its secretion from blood) are all also under study. Genetic editing tools including clustered regularly interspaced short palindromic repeats/Cas9 are also in preclinical study as a potential PH1 therapeutic.. Novel treatments can reduce the plasma oxalate concentration and urinary oxalate excretion in PH1 patients. Thus, it is possible these approaches will reduce the need for combined kidney and liver transplantation to significantly decrease the morbidity and mortality of affected patients.

Topics: Humans; Hyperoxaluria, Primary; Kidney Calculi; L-Lactate Dehydrogenase; Oxalates; RNA, Small Interfering

Kidney stone disease affects ~10% of the global population and the incidence continues to rise owing to the associated global increase in the incidence of medical conditions associated with kidney stone disease including, for example, those comprising the metabolic syndrome. Considering that the intestinal microbiome has a substantial influence on host metabolism, that evidence has suggested that the intestinal microbiome might have a role in maintaining oxalate homeostasis and kidney stone disease is unsurprising. In addition, the discovery that urine is not sterile but, like other sites of the human body, harbours commensal bacterial species that collectively form a urinary microbiome, is an additional factor that might influence the induction of crystal formation and stone growth directly in the kidney. Collectively, the microbiomes of the host could influence kidney stone disease at multiple levels, including intestinal oxalate absorption and direct crystal formation in the kidneys.

Topics: Gastrointestinal Microbiome; Humans; Incidence; Kidney; Kidney Calculi; Oxalates

Kidney stones constitute a disease of the urinary system of high incidence that has only a few available stone dissolving drugs as treatment options. The mechanism of calcium oxalate stone formation is still largely unclear. Various aspects and theories for initiation and formation of the renal stones have been suggested, and the complex multistep formation process of the kidney stones includes supersaturation, nucleation, growth and aggregation of a crystal, and crystal retention in cells after adhesion. During the initial stage of crystal formation, high concentrations of oxalate exposure may damage the renal tubular cells and cause oxidative stress after which the cells may be attached to the crystal thus supporting the oxalate-induced injury as the driving factor of crystal precipitation and cellular adhesion. However, at present, although various drugs targeting kidney stones have been proposed and evaluated both in vitro and in vivo, clinical drugs for stone dissolution have rarely been explored. Moreover, numerous advances in renal calcium oxalate stone associated target and drugs warrant their summarization until now, which could be further discussed and may provide potential ideas or options for exploration of renal calcium oxalate stone treatment targets and drugs.

Topics: Calcium; Calcium Oxalate; Crystallization; Humans; Kidney; Kidney Calculi; Oxalates

The association of kidney stone disease (KSD) and gastrointestinal (GI) surgery has been well established. With a rising obesity crisis, we wanted to see the correlation of urinary composition in patients undergoing bariatric surgery and their risk of KSD. The objective of this paper is to perform a systematic review and meta-analysis of literature to evaluate the changes in urinary composition and risk of KSD following bariatric surgery.. A total of seven studies (2498 patients) underwent bariatric surgery with a mean age of 46.7 years and a male:female ratio of 1:3. The most popular bariatric surgery was the Roux-en-Y procedure. Meta-analysis of the studies showed that significant decrease in urinary calcium, citrate, and urate, and increase in urinary oxalate. There was also a nonsignificant volume reduction in the post-operative cohort. The decrease in urinary citrate and increase in urinary oxalate are both predisposing factors of stone formation. There is strong evidence that bariatric surgery results in significant changes in urine composition in keeping with the increased risk of developing KSD. This identifies useful therapeutic targets in the prophylactic management of patients who have undergone bariatric surgery.

Topics: Bariatric Surgery; Citric Acid; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

Nephrolithiasis is the most common type of urinary system disease in developed countries, with high morbidity and recurrence rates. Nephrolithiasis is a serious health problem, which eventually leads to the loss of renal function and is closely related to hypertension. Modern medicine has adopted minimally invasive surgery for the management of kidney stones, but this does not resolve the root of the problem. Thus, nephrolithiasis remains a major public health issue, the causes of which remain largely unknown. Researchers have attempted to determine the causes and therapeutic targets of kidney stones and calculus‑related hypertension. Solute carrier family 26 member 6 (SLC26A6), a member of the well‑conserved solute carrier family 26, is highly expressed in the kidney and intestines, and it primarily mediates the transport of various anions, including OXa

Topics: Citrates; Dicarboxylic Acid Transporters; Hyperoxaluria; Hypertension; Intestines; Kidney; Kidney Calculi; Membrane Transport Proteins; Nephrolithiasis; Organic Anion Transporters, Sodium-Dependent; Oxalates; Sulfate Transporters; Symporters

Kidney stone disease is a multifactorial condition influenced by both genetic predisposition and environmental factors such as lifestyle and dietary habits. Although different monogenic polymorphisms have been proposed as playing a causal role for calcium nephrolithiasis, the prevalence of these mutations in the general population and their complete pathogenetic pathway is yet to be determined. General dietary advice for kidney stone formers includes elevated fluid intake, dietary restriction of sodium and animal proteins, avoidance of a low calcium diet, maintenance of a normal body mass index, and elevated intake of vegetables and fibers. Thus, balanced calcium consumption protects against the risk for kidney stones by reducing intestinal oxalate availability and its urinary excretion. However, calcium supplementation given between meals might increase urinary calcium excretion without the beneficial effect on oxalate. In kidney stone formers, circulating active vitamin D has been found to be increased, whereas higher plasma 25-hydroxycholecalciferol seems to be present only in hypercalciuric patients. The association between nutritional vitamin D supplements and the risk for stone formation is currently not completely understood. However, taken together, available evidence might suggest that vitamin D administration worsens the risk for stone formation in patients predisposed to hypercalciuria. In this review, we analyzed and discussed available literature on the effect of calcium and vitamin D supplementation on the risk for kidney stone formation.

Topics: Bone and Bones; Calcium; Dietary Supplements; Humans; Hypercalciuria; Intestines; Kidney Calculi; Minerals; Oxalates; Risk; Vitamin D; Vitamin D3 24-Hydroxylase

Urolithiasis is one of the most common urologic diseases in industrialized societies. More than 80% of renal stones are composed of calcium oxalate, and small changes in urinary oxalate concentrations affect the risk of stone formation. Elucidation of the source of oxalate and its mechanism of transport is crucial for understanding the etiology of urolithiasis. Sources of oxalate can be both endogenous and exogenous. With regard to oxalate transport, tests were carried out to prove the function of solute-linked carrier 4 (SLC4) and SLC26. The molecular mechanism of urolithiasis caused by SLC4 and SLC26 is still unclear. The growing number of studies on the molecular physiology of SLC4 and SLC26, together with knockout genetic mouse model experiments, suggest that SLC4 and SLC26 may be a contributing element to urolithiasis. This review summarizes recent research on the sources of oxalate and characterization of the oxalate transport ionic exchangers SLC4 and SLC26, with an emphasis on different physiological defects in knockout mouse models including kidney stone formation. Furthermore, SLC4 and SLC26 exchangers provide new insight into urolithiasis and may be a novel therapeutic target for modification of urinary oxalate excretion.

Topics: Animals; Calcium Oxalate; Humans; Hyperoxaluria; Kidney Calculi; Membrane Transport Proteins; Mice; Oxalates; Sulfate Transporters; Urolithiasis

The review of potential therapies in the treatment of hyperoxaluria is timely, given the current excitement with clinical trials and the mounting evidence of the importance of oxalate in both kidney stone and chronic kidney disease.. Given the significant contribution of both endogenous and dietary oxalate to urinary oxalate excretions, it is not surprising therapeutic targets are being studied in both pathways. This article covers the existing data on endogenous and dietary oxalate and the current targets in these pathways.. In the near future, there will likely be therapies targeting both endogenous and dietary oxalate, especially in subsets of kidney stone formers.

Topics: Adult; Animals; Diet; Humans; Hyperoxaluria; Kidney Calculi; Mice; Oxalates; Rats; Renal Insufficiency, Chronic

Increased level of oxalates in urine and plasma can be attributed to endogenous overproduction, increased ingestion or excessive intestinal absorption. When a supersaturation status is reached, oxalates combine with calcium and crystallize to form 80% of the urinary stones. Several cardiovascular diseases such as coronary heart disease and stroke are thought to be associated with the formation of urinary stones via sharing the same pathogenesis and/or risk factors. This review investigated the evidence linking oxalates/urinary stones to cardiovascular diseases. Eventually, two theories can explain the possible association between urinary stones and cardiovascular diseases: the theory of common origin and the theory of common risk factors. While the first theory is based on the common vascular pathophysiology of urinary stones and cardiac events, the later suggests that metabolic syndrome traits increase the risk of urinary stones and cardiovascular diseases independently. A few cohort studies showed a higher risk of coronary heart disease and stroke among people with history of urinary stones than people without it while other cohort studies did not. These studies had different definitions for cardiovascular diseases, used various methods to assess urinary stones, and some of them did not control for potential confounders. When they were pooled together in meta-analyses, a significant heterogeneity across studies was observed. In conclusion, although there is some evidence indicating that urinary stones could increase the risk of cardiovascular diseases, a substantial causal relationship cannot be settled.

Topics: Cardiovascular Diseases; Humans; Kidney Calculi; Oxalates; Urinary Calculi; Urolithiasis

Both chronic kidney disease (CKD) and kidney stones are major public health problems, which are closely interrelated. Recurrent kidney stones predispose to CKD although CKD seems to decrease risk of further kidney stone formation. Herein, we review new information of this interrelationship.. Several epidemiological studies in the past have shown an association between history of kidney stones and risk for CKD and CKD progression. Recent literature supports this concept and it is reviewed in this article. The issue of whether CKD protects against new kidney stone formation remains unsettled and there is no recent literature addressing it. In relation to stone risk factors in CKD, there are several interesting new articles that discuss mechanisms of hypocitraturia in early CKD before overt metabolic acidosis. Since hypocitraturia is an important risk factor for kidney stone formation we addressed these new data in detail. There are also new data supporting urinary oxalate excretion as a predictor of CKD progression.. It seems clear that recurrent kidney stones should be avoided not only because of their immediate clinical manifestations but also because of their long-term predisposition to CKD progression. Mechanisms leading to hypocitraturia in early CKD still remain controversial.

Topics: Citric Acid; Humans; Kidney Calculi; Oxalates; Renal Insufficiency, Chronic

Kidney stone disease is increasing in prevalence, and the most common stone composition is calcium oxalate. Dietary oxalate intake and endogenous production of oxalate are important in the pathophysiology of calcium oxalate stone disease. The impact of dietary oxalate intake on urinary oxalate excretion and kidney stone disease risk has been assessed through large cohort studies as well as smaller studies with dietary control. Net gastrointestinal oxalate absorption influences urinary oxalate excretion. Oxalate-degrading bacteria in the gut microbiome, especially

Topics: Bacteria; Calcium Oxalate; Diet; Gastrointestinal Microbiome; Humans; Kidney; Kidney Calculi; Nephrolithiasis; Oxalates; Oxalobacter formigenes; Urolithiasis

Primary hyperoxaluria (PH) is caused by genetic mutations resulting in oxalate overproduction leading to nephrolithiasis, nephrocalcinosis, extrarenal manifestations, chronic kidney disease, and end-stage renal disease. Advances in genetic testing techniques have improved our ability to efficiently and effectively obtain a definitive diagnosis of PH as well as easily screen at-risk family members. Similarly, advances in technologies related to intervening at the genetic and molecular level promise to change the way we treat patients with PH. In this review, we provide an update regarding the identification of underlying molecular and biochemical causes of inherited hyperoxalurias, clinical manifestations, and treatment strategies.

Topics: Alcohol Oxidoreductases; Fluid Therapy; Genetic Testing; Humans; Hyperoxaluria, Primary; Kidney Calculi; Kidney Transplantation; Lithotripsy; Liver Transplantation; Mutation; Nephrocalcinosis; Oxalates; Oxo-Acid-Lyases; Pyridoxine; Renal Replacement Therapy; Transaminases; Treatment Outcome

Dietary oxalate is plant-derived and may be a component of vegetables, nuts, fruits, and grains. In normal individuals, approximately half of urinary oxalate is derived from the diet and half from endogenous synthesis. The amount of oxalate excreted in urine plays an important role in calcium oxalate stone formation. Large epidemiological cohort studies have demonstrated that urinary oxalate excretion is a continuous variable when indexed to stone risk. Thus, individuals with oxalate excretions >25 mg/day may benefit from a reduction of urinary oxalate output. The 24-h urine assessment may miss periods of transient surges in urinary oxalate excretion, which may promote stone growth and is a limitation of this analysis. In this review we describe the impact of dietary oxalate and its contribution to stone growth. To limit calcium oxalate stone growth, we advocate that patients maintain appropriate hydration, avoid oxalate-rich foods, and consume an adequate amount of calcium.

Topics: Calcium; Calcium Oxalate; Calcium, Dietary; Diet; Humans; Kidney Calculi; Oxalates

The effect of the intestinal microbiome on urine chemistry and lithogenicity has been a popular topic. Here we review the evidence for exposure to antibiotics increasing the risk of nephrolithiasis.. Studies of the intestinal microbiome have focused on Oxalobacter formigenes, an anaerobe that frequently colonizes the human colon. As a degrader of fecal oxalate its presence is associated with lower urinary oxalate, which would be protective against calcium oxalate stone formation. It also appears capable of stimulating colonic oxalate secretion. A recent study showed that antibiotics can eliminate colonization with O. formigenes. In a case-control study, exposure to sulfa drugs, cephalosporins, fluoroquinolones, nitrofurantoin/methenamine, and broad spectrum penicillins prospectively increased the odds of nephrolithiasis. The effect was greatest for those exposed at younger ages and 3-6 months before being diagnosed with nephrolithiasis.. Recent evidence suggests a possible, causal role of antibiotics in the development of kidney stones. A possible explanation for this finding includes alterations in the microbiome, especially effects on oxalate-degrading bacteria like O. formigenes. Ample reasons to encourage antibiotic stewardship already exist, but the possible role of antibiotic exposure in contributing to the increasing prevalence of kidney stones in children and adults is another rationale.

Topics: Anti-Bacterial Agents; Antimicrobial Stewardship; Gastrointestinal Microbiome; Humans; Kidney Calculi; Oxalates; Oxalobacter formigenes; Risk

The prevalence of kidney stones and cardiovascular diseases (CVDs) are increasing throughout the world. Both diseases are chronic and characterized by accumulation of oxidized proteins and lipids in the renal tissue and arterial wall, respectively. Emerging studies have revealed a positive association between nephrolithiasis and CVDs. Based on preclinical and clinical evidences, this review discusses: (i) stone forming risk factors, crystal nucleation, aggregation, injury-induced crystal retention, and stone formation, (ii) CVD risk factors such as dyslipidemia, perturbation of gut microbiome, obesity, free radical-induced lipoprotein oxidation, and retention in the arterial wall, subsequent foam cell formation, and atherosclerosis, (iii) mechanism by which stone forming risk factors such as oxalate, calcium, uric acid, and infection contribute toward CVDs, and (iv) how CVD risk factors, such as cholesterol, phospholipids, and uric acid, contribute to kidney stone formation are described.

Topics: Animals; Arteries; Atherosclerosis; Calcium; Crystallization; Humans; Kidney; Kidney Calculi; Lipids; Oxalates; Oxidation-Reduction; Plaque, Atherosclerotic; Prevalence; Prognosis; Proteins; Risk Factors; Uric Acid

Short bowel syndrome (SBS) occurs in patients who have had extensive resection. The primary physiologic consequence is malabsorption, resulting in fluid and electrolyte abnormalities and malnutrition. Nutrient digestion, absorption, and assimilation may also be diminished by disturbances in the production of bile acids and digestive enzymes. Small bowel dilation, dysmotility, loss of ileocecal valve, and anatomical changes combined with acid suppression and antimotility drugs increase the risk of small intestinal bacterial overgrowth, further contributing to malabsorption. Metabolic changes that occur in SBS due to loss of colonic regulation of gastric and small bowel function can also lead to depletion of calcium, magnesium, and vitamin D, resulting in demineralization of bone and the eventual development of bone disease. Persistent inflammation, steroid use, parenteral nutrition, chronic metabolic acidosis, and renal insufficiency may exacerbate the problem and contribute to the development of osteoporosis. Multiple factors increase the risk of nephrolithiasis in SBS. In the setting of fat malabsorption, increased free fatty acids are available to bind to calcium, resulting in an increased concentration of unbound oxalate, which is readily absorbed across the colonic mucosa where it travels to the kidney. In addition, there is an increase in colonic permeability to oxalate stemming from the effects of unabsorbed bile salts. The risk of nephrolithiasis is compounded by volume depletion, metabolic acidosis, and hypomagnesemia, resulting in a decrease in renal perfusion, urine output, pH, and citrate excretion. This review examines the causes and treatments of small intestinal bacterial overgrowth, bone demineralization, and nephrolithiasis in SBS.

Topics: Bacteria; Bone and Bones; Bone Density; Calcium; Colon; Humans; Intestinal Mucosa; Intestine, Small; Kidney; Kidney Calculi; Osteoporosis; Oxalates; Short Bowel Syndrome

Nephrolithiasis is a condition marked by the presence or formation of stones in kidneys. Several factors contribute to kidney stones development such as environmental conditions, type of dietary intake, gender and gastrointestinal flora. Most of the kidney stones are composed of calcium phosphate and calcium oxalate, which enter in to the body through diet. Both sources of oxalates become dangerous when normal flora of gastrointestinal tract is disturbed. Oxalobacter and Lactobacillus species exist symbiotically in the human gut and prevent stone formation by altering some biochemical pathways through production of specific enzymes which help in the degradation of oxalate salts. Both Oxalobacter and Lactobacillus have potential probiotic characteristics for the prevention of kidney stone formation and this avenue should be further explored.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Diet; Dietary Supplements; Gastrointestinal Microbiome; Gastrointestinal Tract; Humans; Kidney Calculi; Lactobacillus; Nephrolithiasis; Oxalates; Oxalobacter formigenes; Probiotics

The intestine exerts a considerable influence over urinary oxalate in two ways, through the absorption of dietary oxalate and by serving as an adaptive extra-renal pathway for elimination of this waste metabolite. Knowledge of the mechanisms responsible for oxalate absorption and secretion by the intestine therefore have significant implications for understanding the etiology of hyperoxaluria, as well as offering potential targets for future treatment strategies for calcium oxalate kidney stone disease. In this review, we present the recent developments and advances in this area over the past 10 years, and put to the test some of the new ideas that have emerged during this time, using human and mouse models. A key focus for our discussion are the membrane-bound anion exchangers, belonging to the SLC26 gene family, some of which have been shown to participate in transcellular oxalate absorption and secretion. This has offered the opportunity to not only examine the roles of these specific transporters, revealing their importance to oxalate homeostasis, but to also probe the relative contributions made by the active transcellular and passive paracellular components of oxalate transport across the intestine. We also discuss some of the various physiological stimuli and signaling pathways which have been suggested to participate in the adaptation and regulation of intestinal oxalate transport. Finally, we offer an update on research into Oxalobacter formigenes, alongside recent investigations of other oxalate-degrading gut bacteria, in both laboratory animals and humans.

Topics: Animals; Biological Transport; Humans; Hyperoxaluria; Intestinal Absorption; Intestinal Mucosa; Kidney Calculi; Oxalates

Dietary modifications should be considered as a first line approach in the treatment of idiopathic calcium oxalate nephrolithiasis. The amounts of oxalate and calcium consumed in the diet are significant factors in the development of the disease due to their impact on urinary oxalate excretion. There are a number of strategies that can be employed to reduce oxalate excretion. The consumption of oxalate-rich foods should be avoided and calcium intake adjusted to 1000-1200 mg/day. To encourage compliance it should be emphasized to patients that they be vigilant with this diet as a deviation in any meal or snack could potentially result in significant stone growth. The evidence underlying these two modifications is outlined and other strategies to reduce urinary oxalate excretion are reviewed.

Topics: Calcium Oxalate; Calcium, Dietary; Humans; Intestinal Absorption; Kidney Calculi; Oxalates; Oxalobacter formigenes

Renal urolithiasis is a pathological condition common to a multitude of genetic, physiological and nutritional disorders, ranging from general hyperoxaluria to obesity. The concept of quickly dissolving renal uroliths via chemolysis, especially calcium-oxalate kidney stones, has long been a clinical goal, but yet to be achieved. Over the past 25 years, there has been a serious effort to examine the prospects of using plant and microbial oxalate-degrading enzymes known to catabolize oxalic acid and oxalate salts. While evidence is emerging that bacterial probiotics can reduce recurrent calcium-oxalate kidney stone disease by lowering systemic hyperoxaluria, the possible use of free oxalate-degrading enzyme therapy remains a challenge with several hurdles to overcome before reaching clinical practice.

Topics: Calcium Oxalate; Carboxy-Lyases; Gastrointestinal Microbiome; Humans; Kidney Calculi; Oxalates; Oxalobacter formigenes; Probiotics; Recurrence

Enteric hyperoxaluria is a common occurrence in the setting of fat malabsorption, usually due to intestinal resection or intestinal bypass surgery. Enhanced intestinal absorption of dietary oxalate leads to elevated renal oxalate excretion, frequently in excess of 100 mg/d (1.14 mmol/d). Patients are at increased risk of urolithiasis and loss of kidney function from oxalate nephropathy. Fat malabsorption causes increased binding of diet calcium by free fatty acids, reducing the calcium available to precipitate diet oxalate. Delivery of unabsorbed bile salts and fatty acids to the colon increases colonic permeability, the site of oxalate hyper-absorption in enteric hyperoxaluria. The combination of soluble oxalate in the intestinal lumen and increased permeability of the colonic mucosa leads to hyperoxaluria. Dietary therapy consists of limiting oxalate and fat intake. The primary medical intervention is the use of oral oxalate binding agents such as calcium salts to reduce free intestinal oxalate levels. Bile acid sequestrants can be useful in patients with ileal resection and bile acid malabsorption. Oxalate degrading bacteria provided as probiotics are being investigated but as of yet, no definite benefit has been shown with currently available preparations. The current state of medical therapy and potential future directions will be summarized in this article.

Topics: Bile Acids and Salts; Diet; Fats; Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Malabsorption Syndromes; Oxalates; Oxalobacter formigenes

Nephrolithiasis is a complex disease of worldwide prevalence that is influenced by both genetic and environmental factors. About 75% of kidney stones are predominantly composed of calcium oxalate and urinary oxalate is considered a crucial risk factor. Microorganisms may have a role in the pathogenesis and prevention of kidney stones and the involvement of the intestinal microbiome in this renal disease has been a recent area of interest. Oxalobacter formigenes is a gram negative bacteria that degrades oxalate in the gut decreasing urinary oxalate excretion. In this review, we examine the data studying the role of Oxalobacter formigenes in kidney stone disease in humans and animals, the effect of antibiotics on its colonization, and the potential role of probiotics and whole microbial communities as therapeutic interventions.

Topics: Animals; Anti-Bacterial Agents; Calcium Oxalate; Gastrointestinal Microbiome; Humans; Kidney Calculi; Oxalates; Oxalobacter formigenes; Probiotics; Risk Factors

Oxalate is a highly insoluble metabolic waste excreted by the kidneys. Disturbances of oxalate metabolism are encountered in enteric hyperoxaluria (secondary to malabsorption, gastric bypass or in case of insufficient Oxalobacter colonization), in hereditary hyperoxaluria and in intoxication (ethylene glycol, vitamin C). Hyperoxaluria causes a large spectrum of diseases, from isolated hyperoxaluria to kidney stones and nephrocalcinosis formation, eventually leading to kidney failure and systemic oxalosis with life-threatening deposits in vital organs. New causes of hyperoxaluria are arising recently, in particular after gastric bypass surgery, which requires regular and preemptive monitoring. The treatment of hyperoxaluria involves reduction in oxalate intake and increase in calcium intake. Optimal urine dilution and supplementation with inhibitors of kidney stone formation (citrate) are required. Some conditions may need vitamin B6 supplementation, and the addition of probiotics might be useful in the future. Primary care physicians should identify cases of recurrent calcium oxalate stones and severe hyperoxaluria. Further management of hyperoxaluria requires specialized care.. Oxalat ist ein schwer wasserlösliches Stoffwechselprodukt, das durch die Nieren ausgeschieden wird. Störungen des Oxalatstoffwechsels treten in Form von intestinaler Hyperoxalurie (sekundär infolge Malabsorption, Magen-Bypass oder bei ungenügender Oxalobacter-Kolonisation), hereditärer Hyperoxalurie und als Intoxikationen (Ethylenglykol, Vitamin C) auf. Hyperoxalurie verursacht ein breites Spektrum von Krankheiten von isolierter Hyperoxalurie bis zu Nierensteinen und Nephrokalzinosebildung, was schliesslich zu Nierenversagen und systemischer Oxalose mit lebensbedrohlichen Ablagerungen in wichtigen Organen führen kann. Eine neue Ursache der Hyperoxalurie entstand mit der Magenbypass-Operation, die eine regelmässige und präemptive Überwachung erfordert. Die Behandlung einer Hyperoxalurie besteht in der Reduktion der Oxalataufnahme und in der Erhöhung der Kalziumzufuhr. Eine optimale Urinverdünnung und Supplementierung mit Inhibitoren der Nierensteinbildung (Zitrat) sind erforderlich. Spezifische Fälle können eine Vitamin-B6-Supplementierung und Zugabe von Probiotika erforderlich machen. Hausärzte sollten Fälle von rezidivierenden Kalziumoxalatsteinen und schwerer Hyperoxalurie erkennen und an spezialisierte Zentren weiterleiten.. L'oxalate est un déchet métabolique peu soluble excrété par les reins, et les hyperoxaluries peuvent être distinguées en hyperoxaluries entériques, hyperoxaluries héréditaires et les intoxications (éthylène glycol, vitamine C). L'hyperoxalurie induit un large spectre de maladies allant de l'hyperoxalurie isolée, formation de calculs rénaux, voire d'une néphrocalcinose, à l'insuffisance rénale et l'oxalose systémique avec des dépôts s'accumulant dans de nombreux organes. De nouvelles causes d'hyperoxalurie sont apparues ces dernières années, en particulier les hyperoxaluries survenant à la suite d'un bypass gastrique. Le traitement des hyperoxaluries fait intervenir, d'une part, une diminution contrôlée des apports en oxalate et une augmentation des apports en calcium et, d'autre part, une dilution des urines et l'ajout d'inhibiteurs de la lithogenèse (citrate). Dans certaines conditions particulières, une supplémentation en vitamine B6 ou l'utilisation de probiotiques peuvent être envisagées. Le praticien doit rester attentif aux cas de calculs d'oxalate de calcium récidivants ou d'hyperoxalurie sévère et les adresser pour une prise en charge spécialisée et multidisciplinaire.

Topics: Calcium; Diagnosis, Differential; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Intestine, Large; Kidney Calculi; Oxalates; Oxalobacter formigenes; Risk Factors

We summarize the data regarding the associations of individual dietary components with kidney stones and the effects on 24-hour urinary profiles. The therapeutic recommendations for stone prevention that result from these studies are applied where possible to stones of specific composition. Idiopathic calcium oxalate stone-formers are advised to reduce ingestion of animal protein, oxalate, and sodium while maintaining intake of 800 to 1200 mg of calcium and increasing consumption of citrate and potassium. There are few data regarding dietary therapy of calcium phosphate stones. Whether the inhibitory effect of citrate sufficiently counteracts increasing urine pH to justify more intake of potassium and citrate is not clear. Reduction of sodium intake to decrease urinary calcium excretion would also be expected to decrease calcium phosphate stone recurrence. Conversely, the most important urine variable in the causation of uric acid stones is low urine pH, linked to insulin resistance as a component of obesity and the metabolic syndrome. The mainstay of therapy is weight loss and urinary alkalinization provided by a more vegetarian diet. Reduction in animal protein intake will reduce purine ingestion and uric acid excretion. For cystine stones, restriction of animal protein is associated with reduction in intake of the cystine precursor methionine as well as cystine. Reduction of urine sodium results in less urine cystine. Ingestion of vegetables high in organic anion content, such as citrate and malate, should be associated with higher urine pH and fewer stones because the amino acid cystine is soluble in more alkaline urine. Because of their infectious origin, diet has no definitive role for struvite stones except for avoiding urinary alkalinization, which may worsen their development.

Topics: Beverages; Calcium, Dietary; Citric Acid; Dietary Proteins; Energy Intake; Fructose; Humans; Kidney Calculi; Oxalates; Phytic Acid; Potassium, Dietary; Sodium, Dietary

Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modified by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

Topics: Anion Transport Proteins; Antiporters; Humans; Kidney; Kidney Calculi; Liver; Oxalates

Patients with urolithiasis have been increasing in the world, especially morbidity of calcium nephrolithiasis has been increasing in the advanced countries. The changes in the environmental factors including alternation of diet are said to be associated with the increment of morbidity of kidney stone. Idiopathic hypercalciuria is one of the most important risk factor of calcium nephrolithiasis and is classified into absorptive, resorptive, and renal leak. Though the origins of these three types of hypercalciuria are different, increased bone resorption and increased calcium absorption from gut tend to be observed simultaneously. Not only genetic abnormalities in the proteins which are involved in calcium metabolisms but environmental factors such as high sodium intake and chronic acid load caused by increased ingestion of animal protein have been considered to be associated with increased urinary calcium excretion. Renal metabolisms of oxalate and phosphate which are important compositions of calcium containing stone, uric acid as a promoter and citrate as a inhibitor of nephrolithiasis are also described.

Topics: Adenylyl Cyclases; Bone Resorption; Calcium; Citric Acid; Dietary Proteins; Humans; Hypercalciuria; Kidney; Kidney Calculi; Oxalates; Phosphates; Receptors, Calcium-Sensing; Risk Factors; Sodium Chloride, Dietary; Uric Acid

Urolithiasis is a multifactorial disease involving environmental and gentic factors. Calcium-containing stones, which are>90% of all stones, detected most frequently ; however, radically effective prevention and detailed investigation of crystal formation have not been established. Renal stone formation is a complex multistep process that includes supersaturation, crystal nucleation, growth, and aggregation. In the early stage of crystal formation, exposure to high concentrations of oxalate can induce renal tubular cell injury, following crystal attachment to renal tubular cell in which stone matrix proteins or urinary high molecular substances play an important role as a promoter or inhibitor respectively. Recent study speculated that renal macrophage could englobe crystals and might digest them. In this part, we propose the molecular mechanism that has been newly investigated recently, in renal stone formation.

Topics: Agglutination; Animals; Calcium; Calcium Oxalate; Cell Adhesion; Crystallization; Glycoproteins; Humans; Kidney Calculi; Kidney Tubules; Macrophages; Oxalates

Topics: Acidosis; Case Management; Comorbidity; Diet Therapy; Drug-Related Side Effects and Adverse Reactions; Environment; Humans; Kidney Calculi; Oxalates; Pain Management; Risk Factors; Secondary Prevention; Tomography, X-Ray Computed; Uric Acid; Urologic Surgical Procedures

Humans lack the enzymes needed to metabolize endogenous and dietary oxalate, a toxic compound causing hyperoxaluria and calcium oxalate urolithiasis. Oxalate in humans can be eliminated through (1) excretion in urine, (2) forming insoluble calcium oxalate and elimination in feces, or (3) oxalate degradation by gastrointestinal (GIT) microorganisms. In this article, anaerobic oxalate catabolism in gut bacteria is reviewed, and the possible use of these bacteria as probiotics for treating kidney stone disease is evaluated. Oxalobacter formigenes and Lactobacillus and Bifidobacterium species are the best studied in this regard, with oxalate degradation in the lactic acid bacteria being both species- and strain-specific. The GIT oxalate-degrading bacteria express the catabolic enzymes formyl-CoA transferase (Frc) and oxalyl-CoA decarboxylase (Oxc). The genes encoding these proteins are clustered on the genomes and show strong phylogenetic relationships. Clinical trials investigating reduced hyperoxaluria through administering O. formigenes or its enzymes show a promising trend, but the data need confirmation through larger scale, well-controlled trials. Similar studies using Lactobacillus and Bifidobacterium species also show in vivo oxalate reduction, but these data are still controversial. In particular, further investigations need to determine whether there is a direct link between the lack of oxalate-degrading bacteria and hyperoxaluria and whether their absence is a risk factor. Key experiments linking microbial numbers, functional oxalate degradation, molecular analysis of the regulation of the genes involved, and the ability of the bacteria to survive in the gut are crucial elements in identifying suitable probiotics for treating kidney stone disease.

Topics: Bifidobacterium; Gastrointestinal Tract; Humans; Kidney Calculi; Lactobacillus; Oxalates; Phylogeny; Probiotics

Hyperoxaluria is a major risk factor for the formation of calcium oxalate stones, but dietary restriction of oxalate intake might not be a reliable approach to prevent recurrence of stones. Hence, other approaches to reduce urinary oxalate to manage stone disease have been explored. The gut-dwelling obligate anaerobe Oxalobacter formigenes (OF) has attracted attention for its oxalate-degrading property. In this review we critically evaluate published studies and identify major gaps in knowledge. Recurrent stone-formers are significantly less likely to be colonized with OF than controls, but this appears to be due to antibiotic use. Studies in animals and human subjects show that colonization of the gut with OF can decrease urinary oxalate levels. However, it remains to be determined whether colonization with OF can affect stone disease. Reliable methods are needed to detect and quantify colonization status and to achieve durable colonization. New information about oxalate transport mechanisms raises hope for pharmacological manipulation to decrease urinary oxalate levels. In addition, probiotic use of lactic acid bacteria that metabolize oxalate might provide a valid alternative to OF.

Topics: Humans; Hyperoxaluria; Intestines; Kidney Calculi; Oxalates; Oxalobacter formigenes; Risk Factors

Nephrolithiasis is a result of formation and retention of crystals within the kidneys. The driving force behind crystal formation is urinary supersaturation with respect to the stone-forming salts, which means that crystals form when the concentrations of participating ions are higher than the thermodynamic solubility for that salt. Levels of supersaturation are kept low and under control by proper functioning of a variety of cells including those that line the renal tubules. It is our hypothesis that crystal deposition, i.e., formation and retention in the kidneys, is a result of impaired cellular function, which may be intrinsic and inherent or triggered by external stimuli and challenges. Cellular impairment or dysfunction affects the supersaturation, by influencing the excretion of participating ions such as calcium, oxalate and citrate and causing hypercalciuria, hyperoxaluria or hypocitraturia. The production and excretion of macromolecular promoters and inhibitors of crystallization is also dependent upon proper functioning of the renal epithelial cells. Insufficient or ineffective crystallization modulators such as osteopontin, Tamm-Horsfall protein, bikunin, etc. are most likely produced by the impaired cells.

Topics: Animals; Calcium; Cells; Citric Acid; Crystallization; Humans; Kidney; Kidney Calculi; Kidney Tubules; Mucoproteins; Oxalates; Uromodulin

Urolithiasis is a condition that can cause significant morbidity among patients. Dietary manipulations traditionally advised include fluid, protein, oxalate, calcium, citrate, and sodium changes in the diet. Evidence-based practice guidelines suggest that there is not ample evidence to confidently recommend dietary changes, since inadequate studies have been done to quantify the risks of diet in stone formation. While fluid intake patterns have the weightiest evidence in the literature, not even fluid intake meets the guidelines for evidence-based practice. Health care providers should recognize that current patient education is largely based on intuition. It behooves us as clinicians to look critically at all our practices, review the available literature, and question what we believe we know. A summary of available literature is provided to guide the clinician in educating patients in reducing their risk of recurrent calcium oxalate stone disease.

Topics: Ascorbic Acid; Calcium Oxalate; Calcium, Dietary; Citrates; Dehydration; Diet, Protein-Restricted; Diet, Sodium-Restricted; Evidence-Based Medicine; Feeding Behavior; Fluid Therapy; Humans; Information Services; Internet; Kidney Calculi; Nurse's Role; Nutritional Sciences; Obesity; Oxalates; Patient Education as Topic; Phytotherapy; Practice Guidelines as Topic; Recurrence; Risk Factors

Food and nutrition professionals provide medical nutrition therapy for patients with kidney stones. If the stones contain oxalate or the patient has been diagnosed with hyperoxaluria, reduction of dietary oxalate may be appropriate. Differences in oxalate values for a single food may be due to analytical methods, and/or biological variation from several sources, including cultivar, time of harvest, and growing conditions. Bioavailability of food oxalate and, thus, urine oxalate, will also be affected by salt forms of oxalate, food processing and cooking methods, meal composition, and the presence of Oxalabacter formigenes in the patient's gut. Dietary advice for reducing urinary oxalate should include both reduction of dietary oxalate and simultaneous consumption of calcium-rich food or supplement to reduce oxalate absorption.

Topics: Biological Availability; Calcium Oxalate; Calcium, Dietary; Cooking; Food Analysis; Humans; Intestinal Absorption; Kidney Calculi; Oxalates

Urolithiasis has not been extensively researched in the African continent due to a general lack of facilities and resources. Consideration of the few published papers indicates that there are some regions where the occurrence of stones is extremely rare. South Africa is unique in two respects. Firstly, it has both stone-prone and stone-free population groups and secondly, it is an African country in which a fair amount of research has been conducted in this field. These studies have shown that routine urine parameters cannot explain stone rarity, but that structural differences of inhibitory urinary proteins appear to be important. Similarly, the studies have demonstrated that common dietary components cannot necessarily be correlated with urine composition, particularly oxaluria, nor can they necessarily explain stone rarity, but that the role of oxalate-degrading bacteria has the potential to offer explanatory insights. By investigating the factors influencing stone rarity, those affecting stone formation have been concomitantly scrutinized. As a result, it is suggested that a paradigm shift from a focus on pathology to one on physiology is needed in urolithiasis research in general.

Topics: Africa; Bacterial Physiological Phenomena; Calcium; Humans; Immunity, Innate; Intestines; Kidney Calculi; Oxalates; Proteins; South Africa; Urine

Nephrolithiasis is a disease with a high and even rising incidence. It has a high morbidity, generates high costs and has a high recurrence rate. Urinalysis is of importance especially in recurrent stone formers. It allows the identification and quantification of risk factors and the establishment of individual risk profiles. Based on these individual risk profiles, rational therapy for metaphylaxis of kidney stones lowers stone recurrence rates significantly. This review article aims to give a focussed overview of the most important risk factors for kidney stones and reasonable urine tests for evaluation of recurrent kidney stone formers.

Topics: Biomarkers; Calcium; Citrates; Humans; Kidney Calculi; Oxalates; Prognosis; Risk Assessment; Risk Factors; Urinalysis

Renal stones have afflicted humans for millennia but there is still no solution to this problem. This review discusses the laboratory and metabolic aspects of the clinical management of patients with renal stones, both primary and secondary in origin. First, non-pharmacological interventions such as increased fluid intake, decreased protein consumption, dietary changes in sodium, calcium, oxalate, potassium, purine, vitamins, and essential fatty acids are considered. Then specific pharmacological treatment to modify urine calcium, oxalate, urate, citrate, and acidity are considered. Finally, more unusual types of stone are examined.

Topics: Acidosis, Renal Tubular; Calcium; Calcium, Dietary; Citrates; Cystinuria; Diet, Protein-Restricted; Humans; Inflammatory Bowel Diseases; Kidney Calculi; Oxalates; Uric Acid; Urinalysis

The present review assesses the mechanisms by which oxalate-induced alterations in renal cell function may promote stone disease focusing on 1) changes in membrane surface properties that promote the attachment of nascent crystals and 2) changes in the expression/secretion of urinary macromolecules that alter the kinetics of crystal nucleation, agglomeration and growth. The general role of renal cellular injury in promoting these responses and the specific role of urinary oxalate in producing injury is emphasized, and the signaling pathways that lead to the observed changes in cell surface properties and in the viability and growth of renal cells are discussed. Particular attention is paid to evidence linking oxalate-induced activation of cytosolic phospholipase A2 to changes in gene expression and to the activation of a second signaling pathway involving ceramide. The effects of the lipid signals, arachidonic acid, lysophosphatidylcholine and ceramide, on mitochondrial function are considered in some detail since many of the actions of oxalate appear to be secondary to increased production of reactive oxygen molecules within these organelles. Data from these studies and from a variety of other studies in vitro and in vivo were used to construct a model that illustrates possible mechanisms by which an increase in urinary oxalate levels leads to an increase in kidney stone formation. Further studies will be required to assess the validity of various aspects of this proposed model and to determine effective strategies for countering these responses in stone-forming individuals.

Topics: Animals; Cells, Cultured; Crystallization; Cytosol; Humans; Kidney; Kidney Calculi; Oxalates

The role of dietary oxalate in calcium oxalate kidney stone formation remains unclear. However, due to the risk for stone disease that is associated with a low calcium intake, dietary oxalate is believed to be an important contributing factor. In this review, we have examined the available evidence related to the ingestion of dietary oxalate, its intestinal absorption, and its handling by the kidney. The only difference identified to date between normal individuals and those who form stones is in the intestinal absorption of oxalate. Differences in dietary oxalate intake and in renal oxalate excretion are two other parameters that are likely to receive close scrutiny in the near future, because the research tools required for these investigations are now available. Such research, together with more extensive examinations of intestinal oxalate absorption, should help clarify the role of dietary oxalate in stone formation.

Topics: Animals; Calcium Oxalate; Humans; Intestinal Absorption; Kidney Calculi; Models, Biological; Oxalates

Familial aggregations of nephrolithiasis were already noted in the early 19th century and over the intervening years there has been gradual progression in classifying the familial forms of nephrolithiasis. To date, there are at least 10 different monogenic conditions where those affected have a predisposition to nephrolithiasis. However, all of these rare conditions probably account for less than 2% of renal stone formers. This review, rather than considering these clearly defined disorders, concentrates on research into the broad band of stone formers who have a propensity to nephrolithiasis without an obvious discrete genetic basis.

Topics: Calcium; Citrates; Genetic Predisposition to Disease; Humans; Kidney Calculi; Oxalates; Risk

Calcium oxalate is the most common constituent of kidney stones. Increases in urinary oxalate increase risk of calcium oxalate supersaturation more than increases in urinary calcium, as the physiological level of oxalate is about one-fifth to one-tenth that of urinary calcium. Urinary oxalate derives from two sources: endogenous synthesis and diet. Endogenous synthesis is proportional to lean body mass, and cannot be altered by any current treatment. Dietary oxalate is found in all plant foods. A single food may vary 2-15 fold in oxalate content, depending on variety and growth conditions. The salt form of oxalate, whether sodium, potassium, calcium or magnesium is likely to affect absorption, but has been little studied. Absorption of oxalate from food sources typically is 3-8% of its total oxalate in non-stone-forming individuals. Recent research shows that 40-50% of urinary oxalate comes from the diet of healthy individuals consuming typical diets with 150-250 mg/d dietary oxalate. However, a subpopulation of oxalate "hyperabsorbers" is found in most studies of stoneforming patients. It is likely that all stone formers will benefit from reduction of dietary oxalate, but especially hyperoxaluric stone formers.

Topics: Animals; Diet; Humans; Kidney Calculi; Oxalates; Risk Factors

Oxalate is a major component of the most common form of kidney stones--calcium oxalate stones. High concentrations of oxalate promote stone formation in two ways: (1) by providing urinary conditions favorable to the formation of calcium oxalate crystals, and (2) by inducing renal injury that generates cellular debris and promotes crystal nucleation and attachment. Oxalate toxicity is mediated in part by activation of lipid signaling pathways that produce arachidonic acid, lysophospholipids, and ceramide. These lipids disrupt mitochondrial function by increasing reactive oxygen species (ROS), decreasing mitochondrial membrane potential, and increasing mitochondrial permeability. The net response is cytochrome C release, activation of caspases, and apoptosis or necrosis. Not all cells succumb to oxalate toxicity, however, in those cells that don't, ROS and lipid-signaling molecules induce changes in gene expression that allow them to survive and adapt to the toxic insult. The increased expression of immediate early genes (IEGs), osteopontin, extracellular matrix (ECM) proteins, crystallization inhibitors, and chemokines orchestrates a group of cellular responses--including cell proliferation, secretion of kidney stone inhibitory proteins, recruitment of immune cells, and tissue remodeling--that limit accumulation of cell debris or increase the production of inhibitors of calcium oxalate crystallization, thereby limiting stone formation.

Topics: Adaptation, Physiological; Animals; Calcium Oxalate; Gene Expression; Humans; Kidney Calculi; Lipid Metabolism; Mitochondria; Models, Biological; Osteopontin; Oxalates; Reactive Oxygen Species; Sialoglycoproteins

The popularity of vitamin C can be attributed to Linus Pauling who, in the 1970s, recommended the use of vitamin C for the prevention of influenza. Vitamin C has subsequently been used extensively in a wide range of diseases. Ascorbic acid (vitamin C) has been incriminated as a possible risk factor for calcium oxalate stones due to its enzymatic conversion into oxalate. However, this lithogenic role has never been clearly established. Studies evaluating the effect of ascorbic acid on lithogenesis have reported contradictory results. Ascorbic acid has also been extensively used as an urine acidifier for the treatment of chronic or recurrent urinary tract infection. Once again, the data of the literature are contradictory. The purpose of this article was to review the effects of ascorbic acid on lithogenesis and urinary pH based on a review of the literature.

Topics: Ascorbic Acid; Humans; Kidney Calculi; Oxalates

The major contribution of hypercalciuria in raising urinary state of saturation with respect to calcium salts and subsequent risk of nephrolithiasis is appreciated. Derangements in the physiological mechanisms that regulate calcium homeostasis and contribute to hypercalciuria have also been identified. New avenues of research are beginning to explore the specific defects that may contribute to hypercalciuria. From such studies, an understanding of the role of certain dietary excesses as contributors to the development of hypercalciuria and, in some cases, attendant bone loss, is beginning. The contribution of genetics to hypercalciuria has provided a powerful means of identifying genes that contribute to the hypercalciuric phenotype in a number of hypercalciuric conditions. Such studies have disclosed that hypercalciuria is probably polygenic in nature and will require a concerted effort to better understand the defects while attempting to develop gene-specific countermeasures.

Topics: Calcium; Humans; Kidney Calculi; Lithiasis; Oxalates

Topics: Calcium; Child; Child, Preschool; Cystine; Female; Hematuria; Humans; Kidney Calculi; Magnesium Compounds; Male; Metabolic Diseases; Oxalates; Phosphates; Struvite; Uric Acid; Urinalysis; Urinary Calculi; Urinary Tract Infections

Formation of calcium oxalate (CaOx) kidney stones was investigated using three approaches.. Pathogenesis of crystalluria and crystal deposition in the kidneys was examined in vivo by inducing hyperoxaluria in rats. Cultures of LLC-PK1 and MDCK cells were exposed to oxalate (Ox) and CaOx crystals to examine the effect on cells in various sections of the renal tubules. The nucleation potential of various substrates was examined by incubating them in metastable solutions of CaOx.. Calcium oxalate crystals and nonphysiologic levels of Ox were injurious to renal epithelial cells. To combat these nephrotoxins, renal epithelial cells produce a variety of macromolecules such as bikunin and osteopontin, which are modulators of crystallization and may also be involved in crystal attachment to the cells. Sustained hyperoxaluria in association with CaOx crystals induced apoptosis as well as necrosis. Cellular degradation products induced heterogeneous nucleation of crystals at lower and physiologic levels of oxalate. They also promoted aggregation.. Crystals begin to form in earlier segments of the nephron with a chance to grow and be retained in the collecting ducts after aggregation with other large crystals. Crystal deposits in the collecting ducts near the papillary surface, when exposed to the renal pelvic urine, become nidi for the development of kidney stones.

Topics: Animals; Calcium Oxalate; Cell Aggregation; Cell Line; Crystallization; Dogs; Ethylene Glycol; Humans; Hyperoxaluria; Kidney; Kidney Calculi; Kidney Tubules; Lipid Peroxidation; Membrane Glycoproteins; Necrosis; Osteopontin; Oxalates; Rats; Sialoglycoproteins; Time Factors; Trypsin Inhibitor, Kunitz Soybean

Nephrolithiasis effects 1% to 5% of the general population in industrialized countries. The majority of stones is made of calcium oxalate. The formation of calcium oxalate nephrolithiasis depends on several factors: hypercalciuria, hyperoxaluria, adhesion of crystals on the surface of renal epithelial cells, quantitative or qualitative deficit of inhibitors of crystallization in urine, intervention of promotors of crystallization. In this review we report the new insights into calcium oxalate stone formation.

Topics: Calcium; Calcium Oxalate; Crystallization; Epithelial Cells; Humans; Kidney; Kidney Calculi; Oxalates

Topics: Calcium; Citric Acid; Cystinuria; Humans; Kidney Calculi; Magnesium Compounds; Oxalates; Phosphates; Struvite; Uric Acid

The development of diagnostic protocols that identify specific risk factors for calcium oxalate nephrolithiasis has led to the formulation of directed medical regimens that are aimed at correcting the underlying metabolic disturbances. Initiation of these treatment programs has reduced markedly the rate of stone formation in the majority of patients who form stones. This article discusses the rationale that underlies the choice of medical therapy for the various pathophysiologic causes of calcium oxalate nephrolithiasis and the appropriate use of available medications.

Topics: Calcium; Calcium Oxalate; Citrates; Diet; Humans; Hydrogen-Ion Concentration; Kidney; Kidney Calculi; Oxalates; Uric Acid

Topics: Animals; Calcium; Cell Membrane; Diet; Erythrocytes; Fatty Acid Desaturases; Fatty Acids; Humans; Ion Transport; Kidney Calculi; Linoleoyl-CoA Desaturase; Membrane Lipids; Oxalates; Oxalic Acid

Even though a certain part of oxalate in the urine derives from metabolized ascorbic acid (AA), the intake of high doses of vitamin C does not increase the risk of calcium oxalate kidney stones due to physiological regulatory factor: gastrointestinal absorption as well as renal tubular reabsorption of AA are saturable processes, and the metabolic transformation of AA to oxalate is limited as well. Older assays for urinary oxalate favored in vitro conversion of AA to oxalate during storage and processing of the samples. Recurrent stone formers and patients with renal failure who have a defect in AA or oxalate metabolism should restrict daily vitamin C intakes to approximately 100 mg. But in the large-scale Harvard Prospective Health Professional Follow-Up Study, those groups in the highest quintile of vitamin C intake (> 1,500 mg/day) had a lower risk of kidney stones than the groups in the lowest quintiles.

Topics: Ascorbic Acid; Calcium Oxalate; Case-Control Studies; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Humans; Intestinal Absorption; Kidney; Kidney Calculi; Male; Oxalates; Renal Insufficiency; Retrospective Studies; Risk Factors

Hyperoxaluria is considered to play a crucial role in calcium oxalate (CaOx) renal stone disease. The amount of oxalate excreted into the urine depends on intestinal absorption, endogenous production, renal clearance and renal tubular transport. Since a primary disorder has not been found so far in most CaOx stone formers and since oxalate is freely filtered at the glomerulus, most studies are presently focussed on alterations in epithelial oxalate transport pathways. Oxalate can be transported across an epithelium by the paracellular (passive) and transcellular (active) pathway. Oxalate transport across cellular membranes is mediated by anion-exchange transport proteins. A defect in the structure of these transport proteins could explain augmented transcellular oxalate transport. Little is known about the physiological regulation of oxalate transport. In this review cellular transport systems for oxalate will be summarized with special attention for the progress that has been made to study oxalate transport in a model of cultured renal tubule cells. Better understanding of the physiological processes that are involved in oxalate transport could yield information on the basis of which it might be possible to design new approaches for an effective treatment of CaOx stone disease.

Topics: Animals; Biological Transport; Calcium Oxalate; Humans; Intestinal Mucosa; Kidney; Kidney Calculi; Methods; Oxalates; Sodium Chloride

Urolithiasis is one of the most frequent causes of morbidity in developed countries and its incidence is close to 5%. In our experience, 67.4% of urinary stones contain calcium oxalate as the main component, and hyperoxaluria plays an important role in the pathophysiology of this type of stone. The mechanisms responsible for the increment in urinary excretion of oxalate could involve oxalic acid synthesis. This increase could be due either to an increment of its endogenous formation or to an exogenous load of its precursors. Furthermore, an increased intestinal oxalate absorption is a frequent cause of hyperoxaluria and urolithiasis. Ingestion of oxalate rich foods, imbalance in the supply of other nutrients that influence oxalic acid absorption and GI disorders with malabsorption and/or decreased degradation of intraluminal oxalate can increase intestinal oxalate transport and cause hyperoxaluria. In this article we review the physiological mechanisms that control the oxalate pool: endogenous synthesis, exogenous supply, intestinal absorption and renal excretion of oxalic acid. We analyze the causes and the pathophysiological mechanisms that increase urinary oxalate excretion. We describe a protocol for the biochemical study of patients with hyperoxaluria and the therapeutic measures to reduce urinary oxalate are reviewed. Finally, possible research that may provide further insight into oxalate metabolism in patients with hyperoxaluria are discussed.

Topics: Aluminum; Forecasting; Humans; Hyperoxaluria; Intestinal Absorption; Kidney; Kidney Calculi; Oxalates; Oxalic Acid; Research; Vitamin B 6 Deficiency

Many studies indicate that up-regulated production of 1,25(OH)2-vitamin D3 (calcitriol) with increased intestinal absorption of calcium is the primary event causing idiopathic hypercalciuria. Thus, a low calcium diet appears to be a straightforward strategy in calcium stone formers with hypercalciuria (HCSF). However, the efficacy of such a regimen has never been established, and lowering calcium intake from 1000 to 400 mg/day further enhances calcitriol production. On a diet chronically restricted in calcium, many stone formers increase their intake of animal flesh protein. The latter is known to increase renal mass, and calcitriol levels indeed are positively correlated with renal mass in animals as well as in HCSF. Thus, low calcium and high animal flesh protein consumption are independent stimuli for further up-regulation of calcitriol production. The rise in calcitriol suppresses parathyroid hormone synthesis thereby diminishing renal tubular calcium reabsorption, and increasing urinary calcium losses. Since calcitriol up-regulation also increases bone resorption, the combination of low calcium and high protein intake is particularly likely to induce negative calcium balance and thus osteopenia. Finally, low calcium intake carries the risk of insufficient intestinal binding of oxalate with subsequent increases in intestinal absorption and urinary excretion of oxalate. Indeed, most recent studies suggest that high amounts of calcium, when ingested simultaneously with oxalate-containing meals, are able to prevent hyperoxaluria during severe oral oxalate loading.

Topics: Calcitriol; Calcium; Calcium, Dietary; Feeding Behavior; Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Oxalates

About 80% of all renal stones contain calcium oxalate and/or calcium phosphate as their main crystalline components. The most important risk factors for increases in calcium oxalate crystallization are low urine volume, hyperoxaluria and hypocitraturia. Hypercalciuria, however, is of secondary importance as a cause of increased crystallization: whereas calcium and oxalate crystallize in a 1:1 ratio, the molar concentration ratio in urine amounts to about 10:1 in favor of calcium. Therefore, increases in urinary calcium will not be followed by a rise in crystallization as long as oxalate remains constant, whereas even the slightest increases in urinary oxalate immediately cause more crystals to precipitate. Thus, low calcium diet is not only unnecessary but is contraindicated since it may cause secondary hyperoxaluria (increased intestinal oxalate absorption) and osteopenia (negative calcium balance). On the other hand, overconsumption of animal protein (meat, poultry, fish) induces more pronounced hyperoxaluria and hypocitraturia and contributes to an overall negative calcium balance. It is, however, only by the interplay of "bad" dietary habits with underlying abnormalities such as up-regulation of calcitriol production, incomplete renal tubular acidosis or defective macromolecular crystallization inhibitors, that people become recurrent calcium renal stone formers.

Topics: Adult; Calcium; Calcium Oxalate; Calcium Phosphates; Calcium, Dietary; Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Risk Factors

Excessive intakes of meat protein, oxalate and potentially sodium, as well as insufficient intakes of vegetables fibers, calcium and fluid all lead to increased urinary crystallization. Renal stone disease, however, does not have to ensue. The underlying condition in a given patient is of paramount importance to allow 'bad eating habits' to lead to nephrolithiasis. Several of these underlying abnormalities have been detected so far from which we recently derived the powder keg and tinderbox theory. Most of the time, the dietary approach to nephrolithiasis allows recurrence of renal stone formation to be prevented. The pharmacological approach should be reserved for refractory cases.

Topics: Allopurinol; Animals; Calcium Oxalate; Calcium, Dietary; Diet; Dietary Fiber; Dietary Proteins; Humans; Kidney Calculi; Meat; Oxalates; Recurrence; Sodium, Dietary; Vegetables

Topics: Crystallization; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Calculi; Male; Oxalates; Oxalic Acid

Topics: Antacids; Benzothiadiazines; Calcium; Cation Exchange Resins; Cellulose; Citrates; Citric Acid; Cystinuria; Diuretics; Humans; Kidney Calculi; Lithotripsy; Magnesium; Oxalates; Penicillamine; Phosphates; Sodium Chloride Symporter Inhibitors; Uric Acid; Urinary Tract Infections; Urine

Clinical and basic research in the field of urolithiasis has developed rapidly in recent years. Progress in extracorporeal shock wave lithotripsy (ESWL) and percutaneous nephrolithotomy (PNL) has brought about a revolution in the surgical treatment of urolithiasis and research at the cellular and molecular level is now expanding. In spite of these advances, however, clinical treatment of urolithiasis remains far from satisfactory. Stone recurrence in many patients cannot be predicted and is beyond control of urologists mainly because the mechanisms of stone formation are still not fully understood. It is necessary to study the process of stone-formation more intensely at the cellular and molecular level, and to strengthen the links between basic and clinical research in the field. In this review, the processes involved in the formation of stones are compared with those involved in normal bio-mineralization and a model of urolithiasis is put forward based on modern systems science. Attention is concentrated on: (a) Directions of research based on physico-chemical theories of stone formation; (b) The role of renal tubular defects in urolithiasis; (c) The role of free radical reactions in stone formation; and (d) Macromolecular abnormalities and their correction.

Topics: Biological Transport, Active; Crystallization; Free Radicals; Humans; Kidney Calculi; Kidney Tubules; Oxalates

Dietary restriction of oxalate intake has been used as therapy to reduce the risk of recurrence of calcium oxalate kidney stones. Although urinary oxalate is derived predominantly from endogenous synthesis, it may also be affected by dietary intake of oxalate and calcium. The risk of increasing urinary oxalate excretion by excessive consumption of dietary oxalate is greatest in individuals with a high rate of oxalate absorption, both with and without overt intestinal disease. Although oxalate-rich foods enhanced excretion of urinary oxalate in normal volunteers, the increase was not proportional to the oxalate content of the food. Only eight foods--spinach, rhubarb, beets, nuts, chocolate, tea, wheat bran, and strawberries--caused a significant increase in urinary oxalate excretion. Restriction of dietary calcium enhances oxalate absorption and excretion, whereas an increase in calcium intake may reduce urinary oxalate excretion by binding more oxalate in the gut. This review of the literature indicates that initial dietary therapy for stone-forming individuals can be limited to the restriction of foods definitely shown to increase urinary oxalate. The effects of oxalate-restricted diets on urinary oxalate should be evaluated by means of laboratory analyses of urine composition. Subsequent long-term therapy can be recommended if beneficial results are obtained from oxalate restriction at an appropriate calcium intake.

Topics: Animals; Calcium Oxalate; Calcium, Dietary; Female; Humans; Intestinal Absorption; Kidney Calculi; Male; Oxalates

Selective medical therapy of nephrolithiasis is highly effective in preventing new stone formation. A remission rate of greater than 80% and an overall reduction in individual stone formation rate of greater than 90% can be obtained in patients with nephrolithiasis. In patients with mild to moderate severity of stone disease, virtually total control of stone disease can be achieved with a remission rate of greater than 95%. The need for stone removal may be dramatically reduced by an effective prophylactic program (Fig 6). Selective pharmacological therapy of nephrolithiasis also encompasses the advantages of overcoming nonrenal complications as well as averting certain side effects that may be caused by nonselective medical therapy. Despite these advantages, it is clear that selective medical therapy cannot provide total control of stone disease. A satisfactory response requires continued, dedicated compliance by patients to the recommended program and a commitment by the physician to provide long-term follow-up and care.

Topics: Calcium; Citrates; Citric Acid; Combined Modality Therapy; Diagnosis, Differential; Diuretics; Gout; Humans; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Oxalic Acid; Parathyroidectomy; Phosphates; Struvite; Uric Acid

Topics: Disease Susceptibility; Humans; Kidney; Kidney Calculi; Kidney Diseases; Oxalates; Oxalic Acid

The epidemic of nephrolithiasis in the developed world in the twentieth century is in part the result of the diet consumed in these affluent nations. High protein intake is probably the most important factor. The patients who develop nephrolithiasis may have an increased calciuric response to diet protein and perhaps to diet sodium. The benefits of dietary modification include not only a tendency to reduce urinary calcium excretion but also increased urinary citrate and reduced urinary oxalate excretion. High fluid intake is also an important component of the therapeutic armamentarium of the physician treating patients with recurrent stone formation. The benefit of dietary therapy in patients with recurrent stone formation has not as yet been rigorously tested in controlled studies. Furthermore, there are few valid clinical studies of various pharmacologic agents such as thiazides, phosphates, allopurinol, and citrate. In the absence of clear-cut advantage of any specific pharmacologic agent, it appears that many patients may benefit from dietary modification rather than embarking on a life-long use of medications to prevent stone recurrences.

Topics: Calcium; Diet; Dietary Proteins; Humans; Hyperoxaluria; Kidney Calculi; Oxalates; Oxalic Acid

Topics: Child; Crystallization; Humans; Kidney; Kidney Calculi; Oxalates; Oxalic Acid

Topics: Calcium; Child; Hematuria; Humans; Kidney Calculi; Oxalates; Oxalic Acid; Uric Acid

Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal sy

Topics: Adult; Aged; Calcium; Colloids; Female; Glycosaminoglycans; Humans; Intestinal Absorption; Jejunoileal Bypass; Kidney Calculi; Kidney Tubules; Kinetics; Male; Middle Aged; Oxalates; Oxalic Acid; Parathyroid Hormone

Topics: Allopurinol; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Oxalates; Recurrence; Ureteral Calculi; Urinary Calculi

Advances in renal lithiasis research have contributed to a better understanding of the many varied factors that contribute to renal calculus formation. Utilizing the newer techniques of ambulatory metabolic evaluation, we can establish a specific diagnosis in 95% of recurrent stone-formers. Since a significant percentage of initial stone-formers will never have a second episode, it is essential to establish the natural history of the patient's stone disease prior to initiating potentially life-long medical therapy. The majority of initial stone-formers can be managed with education concerning modest dietary restrictions and increased fluid intake. For the recurrent stone-former with metabolically active stone disease, it is probably best to design medical therapy to treat the specific urinary chemical abnormality or disease process.

Topics: Acidosis, Renal Tubular; Bacterial Infections; Calcium; Crystallography; Cystinuria; Diuresis; Fluid Therapy; Humans; Intestinal Absorption; Kidney; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Patient Education as Topic; Phosphates; Recurrence; Risk; Struvite; Uric Acid; Urography

The normal value of oxaluria, as determined by gasliquid chromatography, is about 30 mg/24 h. In most cases of renal stone formation (60-70%) the stones are composed of calcium oxalate alone or associated with calcium phosphate. The more evolutive the disease, the higher the oxaluria. The part played by oxaluria in renal stone formation and the need to include its determination in regular examinations of stone formers must be stressed. Treatment of hyperoxaluria is both medicinal and dietetic : control of oxalic acid-rich food intake and reduction of the intestinal absorption of oxalate caused by calcium-deprived diets. The diet must be completed by therapeutic measures aimed at reducing the oxaluria and increasing the urinary factors preventing crystallization.

Topics: Diet; Humans; Kidney Calculi; Oxalates

Topics: Calcium; Citrates; Clinical Trials as Topic; Cystine; Cystinuria; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Oxalic Acid; Uric Acid

Consensus from individual studies and several review articles is that consumption of supplemental vitamin C leads to no significant adverse health effects to humans in general. Individuals who have a history of kidney stone formation and those who experience iron overload should exercise caution before using supplemental vitamin C. Occasionally, individuals experience diarrhea or mild nausea. There is also the possibility that vitamin C taken simultaneously with other drugs may contribute to adverse health effects and that its interference in clinical laboratory tests will mask diagnosis of disease. Few controlled clinical trials exist that conclusively demonstrate the adverse health effects that humans may experience with supplemental vitamin C usage, and before definite conclusions can be made of the health hazards to humans, more clinical trials are required.

Topics: Ascorbic Acid; Drug Interactions; False Negative Reactions; Gastrointestinal Diseases; Humans; Intestinal Absorption; Iron; Kidney Calculi; Oxalates; Risk; Vitamin B 12

Topics: Calcium; Fatty Acids; Humans; Ileal Diseases; Kidney Calculi; Malabsorption Syndromes; Oxalates; Uric Acid

Changes in oxalate excretion (together with changes in urinary volume) constitute the most important factors in altering the probability of renal stone formation. However, investigations on oxalate metabolism have been sparse, perhaps because of the lack of an accurate method for measuring oxalate in biologic fluids. Available data clearly implicate increased urinary oxalate excretion as the etiological factor in stone formation in two groups of patients--those with primary hyperoxaluria and those with gastrointestinal malabsorption. Evidence for the existence of hyperoxaluria in the patient with the "garden" variety of calcium oxalate stones is less persuasive.

Topics: Animals; Biological Transport; Calcium Oxalate; Diet; Gastrointestinal Diseases; Glyoxylates; Humans; Intestinal Absorption; Kidney Calculi; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains; Urinary Calculi

Topics: Calcium; Calcium Oxalate; Humans; Kidney Calculi; Oxalates

Topics: Calcium; Cyclic AMP; Diagnosis, Differential; Female; Humans; Kidney Calculi; Male; Oxalates; Parathyroid Hormone; Phosphorus; Uric Acid

Topics: Acidosis, Renal Tubular; Allopurinol; Benzothiadiazines; Calcium; Calcium, Dietary; Cystinuria; Diuretics; Humans; Hyperparathyroidism; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Penicillamine; Phosphates; Quaternary Ammonium Compounds; Sodium Chloride Symporter Inhibitors; Struvite; Uric Acid

Topics: Amino Acids; Biological Transport; Calcium Oxalate; Cystinuria; Dehydration; Digestive System; Glutamine; Hartnup Disease; Humans; Kidney Calculi; Niacinamide; Oxalates; Solubility; Tryptophan

Topics: Calcium Oxalate; Cations; Cholestyramine Resin; Diet; Food Analysis; Humans; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Kidney Diseases; Lipid Metabolism; Malabsorption Syndromes; Oxalates

Topics: Adult; Arthritis; Cholestasis; Fatty Liver; Female; Humans; Ileum; Jejunum; Kidney Calculi; Liver Cirrhosis; Male; Middle Aged; Obesity; Oxalates; Postoperative Complications; Water-Electrolyte Imbalance

Topics: Adult; Animals; Calcium; Child; Diet; Humans; Kidney Calculi; Metabolism, Inborn Errors; Oxalates; Syndrome

Topics: Adenine Phosphoribosyltransferase; Cystinuria; Glycogen Storage Disease Type I; Humans; Hypoxanthine Phosphoribosyltransferase; Kidney Calculi; Metabolism, Inborn Errors; Orotic Acid; Oxalates; Ribose-Phosphate Pyrophosphokinase; Uric Acid; Xanthine Oxidase; Xanthines

Topics: Adolescent; Benzothiadiazines; Calcium; Child; Child, Preschool; Crystallization; Diuretics; Humans; Infant; Infant, Newborn; Kidney Calculi; Magnesium Oxide; Oxalates; Phosphates; Sodium Chloride Symporter Inhibitors

Management of most patients with calculous disease has been less than ideal in the past. Too often therapeutic efforts were limited to symptomatic calculi. Stones were allowed to pass or were removed, metabolic studies were incomplete, victims were dismissed and forgotten, and prophylactic measures were negligible and usually confined to milk restriction and use of distilled water. More patients were crippled with and died of recurrent calculous disease, urinary infection and progressive renal insufficiency than from any other upper urinary tract abnormality. During the last decade the development of a renal stone clinic at this institution has allowed a nephrourologic approach to the management of urolithiasis. This account of classification, diagnosis and management of the various syndromes associated with urolithiasis is based on the experiences gained during the last decade with this common but ill-understood urologic problem.

Topics: Acidosis, Renal Tubular; Adult; Child, Preschool; Cystinuria; Female; Humans; Hypercalcemia; Intestinal Diseases; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates; Sepsis; Uric Acid; Xanthines

Topics: Allopurinol; Calcium; Calcium Metabolism Disorders; Calcium Phosphates; Calcium, Dietary; Crystallization; Humans; Kidney Calculi; Magnesium Oxide; Oxalates; Phosphates; Pyridoxine; Recurrence; Thiazines; Uric Acid

Topics: Adult; Animals; Benzothiadiazines; Calcium; Chemical Precipitation; Child; Citrates; Crystallization; Diphosphates; Diuretics; Female; Humans; Kidney Calculi; Magnesium; Male; Methylene Blue; Milk; Oxalates; Particle Size; Phosphates; Phosphorus; Sodium Chloride Symporter Inhibitors; Solubility; Urinary Calculi

Topics: Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Phosphates; Urinary Bladder Calculi; Urinary Calculi; Urine

Topics: Bacteria; Bile Acids and Salts; Blind Loop Syndrome; Celiac Disease; Cholelithiasis; Diarrhea; Humans; Ileum; Intestinal Absorption; Intestinal Diseases; Intestine, Small; Kidney Calculi; Malabsorption Syndromes; Oxalates; Postoperative Complications; Vitamin B 12 Deficiency

Topics: Adolescent; Adult; Animals; Calcium; Diet; Dose-Response Relationship, Drug; Female; Food Analysis; Humans; Kidney Calculi; Kidney Tubules; Magnesium; Male; Metabolic Clearance Rate; Nutritional Physiological Phenomena; Oxalates; Phosphorus; Sulfur; Tryptophan

Topics: Age Factors; Aged; Calcium; Child; Child, Preschool; Female; Humans; Infant; Kidney Calculi; Male; Nutrition Disorders; Nutritional Physiological Phenomena; Oxalates; Phosphates; Rural Population; Sex Factors; Urban Population; Uric Acid; Urinary Bladder Calculi; Urinary Calculi

Topics: Animals; Calcinosis; Calcium; Ethylenes; Glycols; Humans; Kidney Calculi; Kidney Diseases; Metabolic Diseases; Methoxyflurane; Oxalates; Uric Acid; Urinary Bladder Calculi

Topics: Acid-Base Equilibrium; Age Factors; Calcium; Cystinuria; Female; Humans; Hypercalcemia; Hyperparathyroidism; Immobilization; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Phosphates; Sex Factors; Uric Acid; Vitamin D

Topics: Africa; Asia; Calcium; Chemical Precipitation; Child; Child, Preschool; Chronic Disease; Depression, Chemical; Ethnicity; Europe; Female; Humans; Infant; Kidney Calculi; Lymphatic Diseases; Magnesium; Male; Methylene Blue; Mucoproteins; Oxalates; Phosphates; Protein Binding; Proteinuria; Recurrence; Sex Factors; Sodium; Solubility; United States; Urinary Bladder Calculi

Topics: Alcohol Oxidoreductases; Glyceric Acids; Glycolates; Humans; Intestinal Absorption; Kidney Calculi; Metabolic Diseases; Metabolism, Inborn Errors; Oxalates; Oxidation-Reduction; Radiography; Serine

Topics: Calcium; Humans; Kidney Calculi; Magnesium; Oxalates; Pyridoxine

Topics: Adolescent; Ascorbic Acid; Biochemical Phenomena; Biochemistry; Child; Classification; Diet; Genetics, Medical; Glycine; Glycolates; Humans; Hyperoxaluria, Primary; Infant; Kidney Calculi; Metabolic Diseases; Metabolism; Nephrocalcinosis; Oxalates; Pathology; Terminology as Topic; Uremia; Urine; Vitamin B 6 Deficiency

Topics: Ammonia; Calcium Metabolism Disorders; Chemistry Techniques, Analytical; Cystinuria; Diagnosis; Humans; Kidney Calculi; Oxalates; Statistics as Topic; Surgical Procedures, Operative; Therapeutics; United States; Urine; Xanthines

Primary hyperoxalurias (PHs) are rare genetic diseases that increase the endogenous level of oxalate, a waste metabolite excreted predominantly by the kidneys and also the gut. Treatments aim to improve oxalate excretion, or reduce oxalate generation, to prevent kidney function deterioration. Oxalobacter formigenes is an oxalate metabolizing bacterium. This Phase III, double-blind, placebo-controlled randomized trial investigated the effectiveness of orally administered Oxabact™, a lyophilized O. formigenes formulation, at reducing plasma oxalate levels in patients suffering from PH.. Subjects (≥ 2 years of age) with a diagnosis of PH and maintained but suboptimal kidney function (mean estimated glomerular filtration rate at baseline < 90 mL/min/1.73 m. Forty-three subjects were screened, 25 were recruited and one was discontinued. At Week 52, O. formigenes was established in the gut of subjects receiving Oxabact. Despite decreasing plasma oxalate level in subjects treated with Oxabact, and stable/increased levels with placebo, there was no significant difference between groups in the primary outcome (Least Squares mean estimate of treatment difference was - 3.80 μmol/L; 95% CI: - 7.83, 0.23; p-value = 0.064). Kidney function remained stable in both treatments.. Oxabact treatment may have stabilized/reduced plasma oxalate versus a rise with placebo, but the difference over 12 months was not statistically significant (p = 0.06). A subtle effect observed with Oxabact suggests that O. formigenes may aid in preventing kidney stones. A higher resolution version of the Graphical abstract is available as Supplementary information.

Topics: Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Calculi; Oxalates; Oxalobacter formigenes

Primary hyperoxaluria type 1 (PH1) is a rare genetic disease that causes progressive kidney damage and systemic oxalosis due to hepatic overproduction of oxalate. Lumasiran demonstrated efficacy and safety in the 6-month primary analysis period of the phase 3, multinational, open-label, single-arm ILLUMINATE-B study of infants and children < 6 years old with PH1 (ClinicalTrials.gov: NCT03905694 (4/1/2019); EudraCT: 2018-004,014-17 (10/12/2018)). Outcomes in the ILLUMINATE-B extension period (EP) for patients who completed ≥ 12 months on study are reported here.. Of the 18 patients enrolled in the 6-month primary analysis period, all entered the EP and completed ≥ 6 additional months of lumasiran treatment (median (range) duration of total exposure, 17.8 (12.7-20.5) months).. Lumasiran treatment was previously reported to reduce spot urinary oxalate:creatinine ratio by 72% at month 6, which was maintained at 72% at month 12; mean month 12 reductions in prespecified weight subgroups were 89%, 68%, and 71% for patients weighing < 10 kg, 10 to < 20 kg, and ≥ 20 kg, respectively. The mean reduction from baseline in plasma oxalate level was reported to be 32% at month 6, and this improved to 47% at month 12. Additional improvements were also seen in nephrocalcinosis grade, and kidney stone event rates remained low. The most common lumasiran-related adverse events were mild, transient injection-site reactions (3 patients (17%)).. Lumasiran treatment provided sustained reductions in urinary and plasma oxalate through month 12 across all weight subgroups, with an acceptable safety profile, in infants and young children with PH1. A higher resolution version of the Graphical abstract is available as Supplementary information.

Topics: Child; Child, Preschool; Humans; Hyperoxaluria, Primary; Infant; Kidney Calculi; Oxalates

Primary hyperoxaluria type 1 (PH1) is a rare genetic disease caused by hepatic overproduction of oxalate that leads to kidney stones, nephrocalcinosis, kidney failure, and systemic oxalosis. Lumasiran, an investigational RNA interference (RNAi) therapeutic agent, reduces hepatic oxalate production by targeting glycolate oxidase.. In this double-blind, phase 3 trial, we randomly assigned (in a 2:1 ratio) patients with PH1 who were 6 years of age or older to receive subcutaneous lumasiran or placebo for 6 months (with doses given at baseline and at months 1, 2, 3, and 6). The primary end point was the percent change in 24-hour urinary oxalate excretion from baseline to month 6 (mean percent change across months 3 through 6). Secondary end points included the percent change in the plasma oxalate level from baseline to month 6 (mean percent change across months 3 through 6) and the percentage of patients with 24-hour urinary oxalate excretion no higher than 1.5 times the upper limit of the normal range at month 6.. A total of 39 patients underwent randomization; 26 were assigned to the lumasiran group and 13 to the placebo group. The least-squares mean difference in the change in 24-hour urinary oxalate excretion (lumasiran minus placebo) was -53.5 percentage points (P<0.001), with a reduction in the lumasiran group of 65.4% and an effect seen as early as month 1. The between-group differences for all hierarchically tested secondary end points were significant. The difference in the percent change in the plasma oxalate level (lumasiran minus placebo) was -39.5 percentage points (P<0.001). In the lumasiran group, 84% of patients had 24-hour urinary oxalate excretion no higher than 1.5 times the upper limit of the normal range at month 6, as compared with 0% in the placebo group (P<0.001). Mild, transient injection-site reactions were reported in 38% of lumasiran-treated patients.. Lumasiran reduced urinary oxalate excretion, the cause of progressive kidney failure in PH1. The majority of patients who received lumasiran had normal or near-normal levels after 6 months of treatment. (Funded by Alnylam Pharmaceuticals; ILLUMINATE-A ClinicalTrials.gov number, NCT03681184.).

Topics: Adolescent; Adult; Child; Creatinine; Double-Blind Method; Female; Glomerular Filtration Rate; Humans; Hyperoxaluria, Primary; Kidney Calculi; Male; Middle Aged; Oxalates; RNA, Small Interfering; RNAi Therapeutics; Young Adult

To determine the effect of a probiotic supplement containing native Lactobacillus acidophilus (L. acidophilus) and Bifidobacterium animalis lactis (B. lactis) on 24-hour urine oxalate in recurrent calcium stone formers with hyperoxaluria. Moreover, the in-vitro oxalate degradation capacity and the intestinal colonization of consumed probiotics were evaluated.. The oxalate degrading activity of L. acidophilus and B. lactis were evaluated in-vitro. The presence of oxalyl-CoA decarboxylase (oxc) gene in the probiotic species was assessed. One hundred patients were randomized to receive the probiotic supplement or placebo for four weeks. The 24-hour urine oxalate and the colonization of consumed probiotics were assessed after weeks four and eight.. Although the oxc gene was present in both species, only L. acidophilus had a good oxalate degrading activity, in-vitro. Thirty-four patients from the probiotic and thirty patients from the placebo group finished the study. The urine oxalate changes were not significantly different between groups (57.21 ± 11.71 to 49.44 ± 18.14 mg/day for probiotic, and 56.43 ± 9.89 to 50.47 ± 18.04 mg/day for placebo) (P = .776). The probiotic consumption had no significant effect on urine oxalate, both in univariable (P = .771) and multivariable analyses (P = .490). The consumed probiotics were not detected in the stool samples of most participants.. Our results showed that the consumption of a probiotic supplement containing L. acidophilus and B. lactis did not affect urine oxalate. The results may be due to a lack of bacterial colonization in the intestine.

Topics: Bifidobacterium animalis; Calcium; Double-Blind Method; Humans; Hyperoxaluria; Kidney Calculi; Lactobacillus; Lactobacillus acidophilus; Oxalates; Probiotics

Topics: Adult; Aged; Calcium; Cross-Sectional Studies; Dehydration; Drinking; Female; Humans; Kidney Calculi; Male; Metallurgy; Middle Aged; Occupational Exposure; Osmolar Concentration; Oxalates; Pilot Projects; Prevalence; Risk Factors; Sodium; Uric Acid; Urine

Hyperoxaluria may result from increased endogenous production or overabsorption of dietary oxalate in the gastrointestinal tract leading to nephrolithiasis and, in some, to oxalate nephropathy and chronic kidney disease. ALLN-177 is an oral formulation of a recombinant, oxalate specific, microbial enzyme oxalate decarboxylase intended to treat secondary hyperoxaluria by degrading dietary oxalate in the gastrointestinal tract, thereby reducing its absorption and subsequent excretion in the urine.. This double-blind, placebo controlled, randomized, cross-over, phase 1 study of ALLN-177 evaluated the tolerability of ALLN-177 and its effect on urinary oxalate excretion in 30 healthy volunteers with hyperoxaluria induced by ingestion of a high oxalate, low calcium (HOLC) diet. The primary end point was the difference in the mean 24-hour urinary oxalate excretion during the ALLN-177 treatment period compared with the placebo treatment period.. The daily urinary oxalate excretion increased in the study population from 27.2 ± 9.5 mg/day during screening to 80.8 ± 24.1 mg/day (mean ± SD) on the HOLC diet before introducing ALLN-177 or placebo therapy for 7 days. Compared to placebo, ALLN-177 treatment reduced urinary oxalate by 11.6 ± 2.7 mg/day, p = 0.0002 (least squares mean ± SD).. In healthy volunteers, with diet-induced hyperoxaluria treatment with ALLN-177, when compared to placebo, significantly reduced urinary oxalate excretion by degrading dietary oxalate in the gastrointestinal tract and thereby reducing its absorption. ALLN-177 may represent a new approach for managing secondary hyperoxaluria and its complications.

Topics: Administration, Oral; Adult; Bacillus subtilis; Bacterial Proteins; Carboxy-Lyases; Cross-Over Studies; Diet; Double-Blind Method; Female; Gastrointestinal Absorption; Healthy Volunteers; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates; Recombinant Proteins; Renal Elimination

To elucidate the safety profile and symptom-modifying effect of Alflutop and diacerein in the treatment of Kellgren-Lawrence Stages II-III knee osteoarthrosis (OA) in patients with oxalate nephropathy and Stages I-II chronic kidney disease (CKD) and to refine the effect of these drugs on urinary syndrome and renal function as compared to a response to nonsteroidal anti-inflammatory drugs--cyclooxygenase inhibitors (diclofenac).. This open-label comparative randomized trial enrolled 86 female patients with Kellgren-Lawrence Stages II-III primary gonarthritis concurrent with oxalate nephropathy and Stages I-II CKD. The patients were randomized into 3 groups: 1) 20 patients took diclofenac sodium 100 mg/day; 2) 30 received a complex pharmaceutical on the basis of glycozaminoglycans Alflutop injection 1 ml per day for 20 days, then 2 ml intraartricular twice weekly in the following month; 3) 36 had diacerein (diaflex, "Rompharm Company") in a dose of 50 mg twice daily for 3 months. On day 30 and day 90 of treatment, the symptom- modifying effect was evaluated from changes in the joint pain and morning stiffness domains of the WOMAC index. Renal function was measured using the estimated glomerular filtration rate (GFR), uric acid clearance (C(ua)), and urinary sediment.. On day 30 of treatment, the patients taking diclofenac were found to have nephrotoxic effects (lower GFR, C(ua), evolving secondary hyperuricemia, progressive proteinuria, emerging microhematuria, elevated urinary levels of total lipid hydroperoxides, and enhanced calcium oxalate crystalluria). Alflutop and diacerein exerted no negative effects on renal function. On day 30 day of treatment, all the patient groups showed a reduction in the WOMAC pain score. The diclofenac group displayed a more marked decrease in the pain score than did the two other groups by day 30. Otherwise by day 90 of therapy with Alflutop and diacerein, the pain scores were reduced by 60 and 67%, respectively, which was similar to those in the diclofenac group by day 30 of a follow-up. By day 30 day of treatment, the stiffness score was also observed to fall in all the groups and achieved even lower values in the Alflutop and diacerein groups compared with diclofenac group.. Alflutop and diacerein used by patients with knee OA do not produce nephrotoxic effects and by day 90 demonstrated similar to diclofenac symptom-modifying effect by reducing pain and stiffness scores. Diclofenac administration contributed to oxalate nephropathy progress.. Цель исследования. Выяснение профиля безопасности и симптом-модицифирующего эффекта Алфлутопа и диацереина при лечении остеоартроза (ОА) коленных суставов II-III стадии по критериям Келлгрена-Лоуренса (Kellgren-Lawrence) у пациентов с оксалатной нефропатией с хронической болезнью почек (ХБП) I-II стадии, уточнение влияния Алфлутопа и диацереина на мочевой синдром и функцию почек в сопоставлении с ответом на нестероидные противовоспалительные средства - ингибиторы циклооксигеназы (диклофенак). Материалы и методы. В открытое сравнительное рандомизированное исследование включены 86 больных женского пола с наличием первичного гоноартроза II-III стадии по критериям Келлгрена-Лоуренса с сопутствующей оксалатной нефропатией с ХБП I-II стадии. Пациенты рандомизированы на 3 группы: в 1-й группе (20 человек) получали диклофенак натрия в дозе 100 мг/сут; во 2-й (30 человек) - Алфлутоп в дозе 1 мл внутримышечно ежедневно в течение 20 дней, затем следующий месяц внутрисуставно - в дозе 2 мл 2 раза в неделю; в 3-й (36 человек) - диацереин (диафлекс, 'Rompharm Company', Болгария) в дозе 50 мг 2 раза в сутки в течение 3 мес. Симптом-модифицирующий эффект оценивали на 30-й и 90-й дни лечения по динамике шкалы суставной боли и утренней скованности по индексу WOMAC. Состояние функции почек определяли по расчетной скорости клубочковой фильтрации (СКФ), клиренсу мочевой кислоты (Кмк) и мочевому осадку. Результаты. К 30-му дню лечения у больных, принимающих диклофенак, выявлены нефротоксические эффекты (снижение СКФ, Кмк, развитие вторичной гиперурикемии, нарастание протеинурии, появление микрогематурии, увеличение в моче общих гидроперекисей липидов, усиление оксалатно-кальциевой кристаллурии). Алфлутоп (комплексный препарат на основе гликозаминогликанов) и диацереин (ингибитор ИЛ-1) не оказали отрицательного влияния на функциональное состояние почек. На 30-й день лечения во всех группах больных было достигнуто снижение боли по индексу WOMAC. В группе, где принимали диклофенак, уменьшение индекса боли было более выражено, чем в двух других. Уровни индексов боли к 90-му дню лечения Алфлутопом и диацереином статистически значимо не различались, снизившись на 60 и 67% соответственно, что сопоставимо с уровнем снижения боли в группе приема диклофенака к 30-му дню наблюдения. Уменьшение индекса скованности также отмечено к 30-му дню лечения во всех группах, а на 90-й день индекс достиг еще более низких значений на фоне приема Алфлутопа и диацереина Заключение. При приеме Алфлутопа

Topics: Anthraquinones; Anti-Inflammatory Agents; Cyclooxygenase Inhibitors; Diclofenac; Dose-Response Relationship, Drug; Double-Blind Method; Drug Therapy, Combination; Female; Follow-Up Studies; Glomerular Filtration Rate; Humans; Injections, Intramuscular; Kidney Calculi; Middle Aged; Osteoarthritis, Knee; Oxalates; Treatment Outcome

To determine whether the ratio of dietary calcium and oxalate consumption at mealtime affects gastrointestinal oxalate absorption and urinary oxalate excretion.. A study was conducted with 10 non-stone-forming adults placed on controlled diets with daily calcium and oxalate contents of 1000 and 750 mg, respectively. Subjects consumed a balanced calcium/oxalate ratio diet for 1 week, observed a minimum 1-week washout period, and subsequently consumed an imbalanced calcium/oxalate ratio diet for one week. Urine specimens were collected on the last 4 days of each diet. Outcome measures included urinary creatinine, calcium, and oxalate as well as the Tiselius index for assessing urinary calcium oxalate supersaturation.. Total daily calcium excretion, oxalate excretion, and Tiselius index were similar between balanced and imbalanced dietary phases. There were significant differences in calcium excretion (mg/g creatinine) between balanced and imbalanced diets in the 1-6 PM (83.1 vs 110.2, P <.04), 6-11 PM (71.3 vs 107.2, P <.02), and 11 PM-8 AM collections (55.0 vs 41.8, P <.02). There was significantly higher oxalate excretion on the balanced diet in the 1-6 pm time period (28.1 vs 16.7, P <.01). There were no differences in the Tiselius index in these collections.. These results demonstrate that the sequence of ingesting relatively large amounts of oxalate does not significantly affect calcium oxalate stone risk if the recommended daily quantity of dietary calcium is consumed.

Topics: Adult; Calcium Oxalate; Calcium, Dietary; Creatinine; Diet; Female; Humans; Intestinal Absorption; Kidney Calculi; Male; Oxalates

Primary hyperoxaluria (PH) is a rare genetic disease, in which high urinary oxalate (Uox) cause recurrent kidney stones and/or progressive nephrocalcinosis, often followed by early end-stage renal disease, as well as extremely high plasma oxalate, systemic oxalosis and premature death. Oxalobacter formigenes, an anaerobic oxalate degrading bacterium, naturally colonizes the colon of most humans. Orally administered O. formigenes (Oxabact) was found to significantly reduce urine and plasma oxalate. We aimed to evaluate its effect and safety in a randomized, double-blind, placebo-controlled multicenter study.. Oral Oxabact was given to PH patients (>5 years old, Uox > 1.0 mmol/1.73 m(2)/day, glomerular filtration rate (GFR) > 50 mL/min) at nine PH referral sites worldwide. Primary endpoint was the change from baseline in Uox (mmol/1.73 m(2)/day) after 24 weeks of treatment (>20% reduction).. Of the 43 subjects randomized, 42 patients received either placebo (23 subjects) or Oxabact (19 subjects). The change in Uox was <20% and not different between groups (P = 0.616). Ad hoc analysis was performed in 37 patients compliant with medication and urine processing. Change in Uox was -19% in subjects given Oxabact and -10% in placebo, (P = 0.288), but -21 and -7% with Uox expressed as molar creatinine ratio (Ox:Cr, mmol/mol, P = 0.06). Reduction of Ox:Cr was more obvious for patients with higher baseline values (>160 mmol/mol, Oxabact -28%, placebo -6%; P < 0.082). No serious adverse events were reported.. Oxabact was safe and well tolerated. However, as no significant change in Uox was seen, further studies to evaluate the efficacy of Oxabact treatment are needed.

Topics: Administration, Oral; Aged; Creatinine; Double-Blind Method; Female; Follow-Up Studies; Glomerular Filtration Rate; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Oxalobacter formigenes; Prognosis

The renal handling and intestinal absorption of dietary oxalate are believed to be risk factors for calcium oxalate stone formation. In this study, we have examined the time and dose effects of soluble oxalate loads on the intestinal absorption and renal handling of oxalate in six stone formers (SF) and six normal individuals (N) who consumed diets controlled in oxalate and other nutrients. Urinary and plasma oxalate changes were monitored over 24 h after ingestion of 0, 2, 4, and 8 mmole oxalate loads, containing a mixture of (12)C- and (13)C(2)-oxalate. There were significant time and dose dependent changes in urinary oxalate excretion and secretion after these loads. However, there were no significant differences between SF and N in both the intestinal absorption and the renal handling of oxalate loads, as measured by the urinary excretion of oxalate (P = 0.96) and the ratio of oxalate to creatinine clearance (P = 0.34). (13)C(2)-oxalate absorption studies showed three of the subjects, two SF and one N, had enhanced absorption with the 8 mmole load. A clear difference in absorption was demonstrated in these individuals during the 8-24 h interval, suggesting that in these individuals there was greater oxalate absorption in the large intestine as compared to the other subjects. This enhanced absorption of oxalate warrants further characterization.

Topics: Administration, Oral; Adult; Biological Transport; Carbon Isotopes; Dose-Response Relationship, Drug; Female; Humans; Intestinal Absorption; Intestinal Mucosa; Kidney; Kidney Calculi; Male; Oxalates; Time Factors

Urinary oxalate excretion is an important contributor to calcium oxalate stone formation. Methods of reducing oxalate excretion are not wholly satisfactory, and no controlled trials using them have been performed to prevent stone recurrence. Some lactic acid bacteria can degrade oxalate in vitro. This study sought to reduce urinary oxalate excretion in calcium stone formers with idiopathic hyperoxaluria.. A randomized, double-blind, placebo-controlled trial was performed of Oxadrop, a mix of four lactic acid bacterium species. This preparation previously reduced oxalate excretion in stone formers with idiopathic and enteric hyperoxaluria. Patients were selected from two stone prevention clinics. Twenty people with calcium stones and idiopathic hyperoxaluria (>40 mg/d) were enrolled and randomly assigned 1:1 in placebo and active preparation arms. Both groups took 3.6 g of granulate each day: Either placebo or the experimental preparation. Participants performed two consecutive 24-h urine collections at baseline, at 28 d of therapy, and at 56 d, after being off the preparation for 4 wk. Diet was replicated at each point.. There was no effect of the study preparation: Mean 24-h urinary oxalate excretion in placebo-treated patients was 73.9 mg at baseline and 72.7 mg after treatment, whereas the Oxadrop-treated patients had 59.1 mg at baseline and 55.4 mg after treatment. The preparation was well tolerated; three participants on active treatment experienced mild constipation.. In this randomized, placebo-controlled trial, Oxadrop did not reduce urinary oxalate excretion in participants with idiopathic hyperoxaluria.

Topics: Bifidobacterium; Biological Therapy; Double-Blind Method; Female; Humans; Hyperoxaluria; Kidney Calculi; Lactic Acid; Lactobacillus acidophilus; Levilactobacillus brevis; Male; Middle Aged; Oxalates; Streptococcus thermophilus

1) To investigate the amount of citrate and tartrate in aloe gel, and in the urine of healthy normal children, before and after consuming fresh aloe gel. 2) To evaluate the changes in the chemical composition of urine among subjects after taking aloe gel. 3) To determine the value of consuming aloe gel for prevention of renal stone formation.. Experimental study.. Thirteen healthy boys between 9 and 13 years of age were enrolled (with informed permission) in the clinical trial. Subjects ingested 100 g of fresh prepared aloe gel twice a day for seven consecutive days. The 24-hour urine was collected one day prior to taking the gel (Day 0), Days 2 and 5 of consumption, and Day 8 (one day after completion). The authors determined the urine volume, osmolality, potassium, sodium, phosphate, calcium, magnesium, uric acid, citrate, tartrate, oxalate, Permissible Increment in Calcium (PI Ca), Permissible Increment in Oxalate (PI Ox), Concentration Product Ratio of Calcium Phosphate (CPR CaPO4) and the citrate per creatinine ratio.. The citrate and tartrate concentration in 100 g of fresh aloe gel was 96.3 and 158.9 mg, respectively. The 24-hr urine volume and urinary citrate excretion were significantly increased (p < 0.05). The PI Ca and the PI Ox were also significantly increased (p < 0.05). The other measurements were unremarkable.. One hundred grams of fresh Aloe vera gel contains 96.3 milligrams of citrate and 158.9 milligrams of tartrate and were in the mid-range among Thai fruits. Changes in chemical compositions of urine after aloe gel consumption shows potential for preventing kidney stone formation among children.

Topics: Administration, Oral; Adolescent; Aloe; Child; Citric Acid; Gels; Humans; Kidney Calculi; Male; Oxalates; Tartrates; Urine

Currently, the recommended upper limit for ascorbic acid (AA) intake is 2000 mg/d. However, because AA is endogenously converted to oxalate and appears to increase the absorption of dietary oxalate, supplementation may increase the risk of kidney stones. The effect of AA supplementation on urinary oxalate was studied in a randomized, crossover, controlled design in which subjects consumed a controlled diet in a university metabolic unit. Stoneformers (n = 29; SF) and age- and gender-matched non-stoneformers (n = 19; NSF) consumed 1000 mg AA twice each day with each morning and evening meal for 6 d (treatment A), and no AA for 6 d (treatment N) in random order. After 5 d of adaptation to a low-oxalate diet, participants lived for 24 h in a metabolic unit, during which they were given 136 mg oxalate, including 18 mg 13C2 oxalic acid, 2 h before breakfast; they then consumed a controlled very low-oxalate diet for 24 h. Of the 48 participants, 19 (12 stoneformers, 7 non-stoneformers) were identified as responders, defined by an increase in 24-h total oxalate excretion > 10% after treatment A compared with N. Responders had a greater 24-h Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66 treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31% increase in the percentage of oxalate absorption (10.5 +/- 3.2% treatment A vs. 8.0 +/- 2.4% treatment N) and a 39% increase in endogenous oxalate synthesis with treatment A than during treatment N (544 +/- 131 A vs. 391 +/- 71 micromol/d N). The 1000 mg AA twice each day increased urinary oxalate and TRI for calcium oxalate kidney stones in 40% of participants, both stoneformers and non-stoneformers.

Topics: Adult; Ascorbic Acid; Body Mass Index; Body Weight; Calcium; Calcium Oxalate; Cross-Over Studies; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Oxalates; Reference Values; Risk Factors

Patients with inflammatory bowel disease have a 10- to 100-fold increased risk of nephrolithiasis, with enteric hyperoxaluria being the major risk factor for these and other patients with fat malabsorptive states. Endogenous components of the intestinal microflora can potentially limit dietary oxalate absorption.. Ten patients were studied with chronic fat malabsorption, calcium oxalate stones, and hyperoxaluria thought to be caused by jejunoileal bypass (1) and Roux-en-Y gastric bypass surgery for obesity (4), dumping syndrome secondary to gastrectomy (2), celiac sprue (1), chronic pancreatitis (1), and ulcerative colitis in remission (1). For 3 months, patients received increasing doses of a lactic acid bacteria mixture (Oxadrop), VSL Pharmaceuticals), followed by a washout month. Twenty-four-hour urine collections were performed at baseline and after each month.. Mean urinary oxalate excretion fell by 19% after 1 month (1 dose per day, P < 0.05), and oxalate excretion remained reduced by 24% during the second month (2 doses per day, P < 0.05). During the third month on 3 doses per day oxalate excretion increased slightly, so that the mean was close to the baseline established off treatment. Urinary oxalate again fell 20% from baseline during the washout period. Calcium oxalate supersaturation was reduced while on Oxadrop, largely due to the decrease in oxalate excretion, although mean changes did not reach statistical significance.. Manipulation of gastrointestinal (GI) flora can influence urinary oxalate excretion to reduce urinary supersaturation levels. These changes could have a salutary effect on stone formation rates. Further studies will be needed to establish the optimal dosing regimen.

Topics: Aged; Bifidobacterium; Humans; Hyperoxaluria; Intestines; Kidney Calculi; Lactobacillus acidophilus; Levilactobacillus brevis; Malabsorption Syndromes; Male; Middle Aged; Oxalates; Probiotics; Streptococcus thermophilus; Treatment Outcome

It has been speculated that calcium supplement in subjects with low oxalate intake might increase the risk of calcium stone formation due to an increase in calcium absorption without a significant reduction in oxalate absorption. There have been no human studies addressing specifically the effects of taking calcium supplements in populations whose dietary oxalate is low. This study was conducted to determine the effects of calcium supplements on the risk of calcium stone formation in a population with low oxalate intake. Thirty-two healthy male navy privates, 22.7 +/- 1.9 (mean +/- SD) years old, who had oxalate intake of less than 1 mmol/day, a serum creatinine of less than 150 micromol/l, and no history of renal stones, participated in the study. Dietary oxalate was controlled to be under 1 mmol/day throughout the study. Twenty-four hour urine collections for the determination of urinary constituents were obtained at baseline and after taking calcium supplements. Detection of calcium oxalate was performed to assess the risk of calcium oxalate stone formation. The urinary excretion of calcium was significantly elevated above baseline values while taking the calcium supplements (3.48 +/- 2.13 vs 5.17 +/- 2.61 mmol/d, p < 0.05) and urinary oxalate was significantly decreased when the subjects took calcium supplements compared to the corresponding baseline value (0.13 +/- 0.05 vs 0.17 +/- 0.07 mmol/d, p = 0.01). Urinary citrate was significantly elevated when the subjects took calcium supplements compared to the baseline (0.83 +/- 0.57 vs 0.64 +/- 0.39 mmol/d, p = 0.03). There was no significant alteration in the activity products of calcium oxalate while taking the calcium supplements (0.54 +/- 0.25 vs 0.57 +/- 0.22, p = 0.54). The effect of calcium supplements with meals, for the reduction of the risk of calcium stone formation, was unchanged, even in a population whose oxalate intake is rather low. Taking calcium supplements resulted in a reduction in urinary oxalates and an elevation in urinary citrates. Both alterations in urinary constituents counterbalanced the elevation in urinary calcium which resulted from the calcium supplements.

Topics: Adult; Calcium, Dietary; Diet; Humans; Kidney Calculi; Male; Oxalates; Risk Factors

To investigate the oxalate intake and the effect of an oxalate load on urinary oxalate excretion in calcium stone-forming (CSF) patients.. Prospective study.. University-affiliated outpatient Renal Lithiasis Unit.. Seventy (70) CSF and 41 healthy subjects (HS) collected a 24-hour urine sample and were submitted to a 3-day dietary record to determine mean oxalate (Ox), calcium (Ca) and vitamin C intake. Fifty-eight (58) CSF patients were randomly selected to receive milk (N = 28) or dark (N = 30) chocolate as an oxalate load.. Administration of either milk (94 mg Ox + 430 mg Ca) or dark chocolate (94 mg Ox + 26 mg Ca) for 3 days. A 24-hour urine sample was obtained before and after the load to determine calcium, oxalate, sodium, potassium, urea, and creatinine.. Oxalate intake and excretion.. CSF patients presented mean Ox intake of 98 +/- 137 mg/d, similar to that of HS (108 +/- 139 mg/d). Mean Ox and vitamin C intake was directly correlated with Ox excretion only in CSF. The consumption of dark chocolate induced a significant increase in mean urinary Ox (36 +/- 14 versus 30 +/- 10 mg/24 hr) not observed in the milk chocolate group. Thus, a 2-fold increase in Ox intake in this population of CSF patients produced a significant 20% increase in oxaluria, not observed when Ca was consumed simultaneously.. The present study suggests that even small increases in Ox intake affect oxalate excretion and the mitigation of urinary oxalate increase by Ca consumption reinforces that Ca and Ox intakes for CSF patients should be in balance. Further studies are necessary to assess whether or not a 20% increase in oxaluria will lead to a higher risk of stone formation.

Topics: Adult; Animals; Ascorbic Acid; Cacao; Calcium; Calcium, Dietary; Diet Records; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Milk; Oxalates

We assessed the effects of thiazide treatment on urine oxalate excretion in patients with kidney stones.. Of 537 patients (231 women), 209 (81 women) received thiazide for stone prevention. Urine oxalate was measured in 3, 24-hour urines before treatment, and in 1, 24-hour urine after 6 to 12 weeks of treatment. This was an observational cohort and treatment was not randomized.. Urine oxalate increased in general. There was no difference in increase with or without thiazide, whether one considered simple t test comparisons or used ANOVA with pretreatment oxalate excretion as a covariate.. Thiazide administration exerts no measurable effect on urine oxalate excretion that can be detected in clinical practice.

Topics: Adult; Benzothiadiazines; Diuretics; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Sodium Chloride Symporter Inhibitors

A low-calcium diet is recommended to prevent recurrent stones in patients with idiopathic hypercalciuria, yet long-term data on the efficacy of a low-calcium diet are lacking. Recently, the efficacy of a low-calcium diet has been questioned, and greater emphasis has been placed on reducing the intake of animal protein and salt, but again, long-term data are unavailable.. We conducted a five-year randomized trial comparing the effect of two diets in 120 men with recurrent calcium oxalate stones and hypercalciuria. Sixty men were assigned to a diet containing a normal amount of calcium (30 mmol per day) but reduced amounts of animal protein (52 g per day) and salt (50 mmol of sodium chloride per day); the other 60 men were assigned to the traditional low-calcium diet, which contained 10 mmol of calcium per day.. At five years, 12 of the 60 men on the normal-calcium, low-animal-protein, low-salt diet and 23 of the 60 men on the low-calcium diet had had relapses. The unadjusted relative risk of a recurrence for the group on the first diet, as compared with the group on the second diet, was 0.49 (95 percent confidence interval, 0.24 to 0.98; P=0.04). During follow-up, urinary calcium levels dropped significantly in both groups by approximately 170 mg per day (4.2 mmol per day). However, urinary oxalate excretion increased in the men on the low-calcium diet (by an average of 5.4 mg per day [60 micromol per day]) but decreased in those on the normal-calcium, low-animal-protein, low-salt diet (by an average of 7.2 mg per day [80 micromol per day]).. In men with recurrent calcium oxalate stones and hypercalciuria, restricted intake of animal protein and salt, combined with a normal calcium intake, provides greater protection than the traditional low-calcium diet.

Topics: Adult; Calcium; Calcium Oxalate; Calcium, Dietary; Diet Therapy; Diet, Sodium-Restricted; Dietary Proteins; Humans; Incidence; Kidney Calculi; Male; Middle Aged; Oxalates; Secondary Prevention

To correlate renal calculi and other clinical factors with urinary biochemical analytes in patients with inflammatory bowel disease, and to investigate the relative importance of hyperoxaluria (associated with fat malabsorption) or reduced stone inhibitors in the development of calculi in these patients.. Samples were obtained from 25 patients with Crohn's disease (CD), 15 with ulcerative colitis (UC) and 17 normal subjects (controls). Evidence for the presence of renal calculi was obtained from plain films, ultrasonography or intravenous urography. Urine oxalate and citrate were analysed using commercial enzymatic assays; magnesium was measured using atomic absorption and other analytes assayed using standard methods on automated analysers.. Renal calculi were found in two patients with CD and in none with UC. Hyperoxaluria was present in 36% of patients with CD but was absent in those with UC. Analysis of covariance showed an association between low urinary citrate/creatinine ratio and renal stones (P=0.02), and between a combined urinary citrate and magnesium deficit relative to calcium, as expressed in the CMC index ((citratexmagnesium)/calcium), and renal stones (P=0.017). Changes in urinary calcium, oxalate, urate, magnesium or the calcium oxalate index were not associated with the presence of stones. There was no independent relationship between any clinical factor and the presence of stones.. Lower urinary concentrations of magnesium and citrate (stone inhibitors), relative to calcium (stone promoter; the CMC index) may be more important in lithogenesis in inflammatory bowel disease than is hyperoxaluria. In patients with a functioning colon, a low CMC index may predict likely stone-formers; this requires a prospective evaluation. Avoiding low urinary levels of magnesium and citrate may aid in preventing and treating renal calculi.

Topics: Acute-Phase Proteins; Adult; Aged; C-Reactive Protein; Citrates; Colitis, Ulcerative; Creatinine; Crohn Disease; Female; Humans; Hyperoxaluria; Kidney Calculi; Magnesium; Malabsorption Syndromes; Male; Middle Aged; Oxalates; Risk Factors; Serum Albumin

High protein intake is an accepted risk factor for renal stone disease. Whether meat protein intake affects oxaluria, however, remains controversial in healthy subjects and in stone formers. This study was designed (1) to test the oxaluric response to a meat protein load in male recurrent idiopathic calcium stone formers (ICSFs) with and without mild metabolic hyperoxaluria (MMH and non-MMH, respectively), as well as in healthy controls, and (2) to seek for possible disturbed vitamin B(6) metabolism in MMH, in analogy with primary hyperoxaluria.. Twelve MMH, 8 non-MMH, and 13 healthy males were studied after five days on a high meat protein diet (HPD; 700 g meat/fish daily) following a run-in phase of five days on a moderate protein diet (MPD; 160 g meat/fish daily). In both diets, oxalate-rich nutrients were avoided, as well as sweeteners and vitamin C-containing medicines. Twenty-four-hour urinary excretion of oxalate was measured on the last day of each period, along with 4-pyridoxic acid (U(4PA)) and markers of protein intake, that is, urea, phosphate, uric acid, and sulfate. Serum pyridoxal 5' phosphate (S(P5P)) was measured after protein loading.. Switching from MPD (0.97 +/- 0.18 g protein/kg/day) to HPD (2.26 +/- 0.38 g protein/kg/day) led to the expected rise in the urinary excretion rates of all markers of protein intake in all subjects. Concurrently, the mean urinary excretion of oxalate increased in ICSFs taken as a whole (+73 +/- 134 micromol/24 h, P = 0.024) as well as in the MMH subgroup (+100 +/- 144 micromol/24 h, P = 0.034) but not in controls (-17 +/- 63 micromol/24 h). In seven ICSFs (4 MMH and 3 non-MMH) but in none of the healthy controls (P = 0.016, chi square), an increment in oxaluria was observed and considered as significant based on the intra-assay coefficient of variation at our laboratory (8.5%). There was no difference in S(P5P)nd U(4PA)etween the groups after protein loading.. Approximately one third of ICSFs with or without so-called MMH are sensitive to meat protein in terms of oxalate excretion, as opposed to healthy subjects. Mechanisms underlying this sensitivity to meat protein remain to be elucidated and do not seem to involve vitamin B(6) deficiency.

Topics: Adult; Calcium; Diet, Protein-Restricted; Dietary Proteins; Glycolates; Humans; Hyperoxaluria; Kidney Calculi; Male; Meat; Middle Aged; Oxalates; Pyridoxal Phosphate; Pyridoxic Acid; Pyridoxine; Sulfates

Hyperoxaluria is a major risk factor for renal stones, and in most cases, it appears to be sustained by increased dietary load or increased intestinal absorption. Previous studies have shown that components of the endogenous digestive microflora, in particular Oxalobacter formigenes, utilize oxalate in the gut, thus limiting its absorption. We tested the hypothesis of whether oxaluria can be reduced by means of reducing intestinal absorption through feeding a mixture of freeze-dried lactic acid bacteria.. Six patients with idiopathic calcium-oxalate urolithiasis and mild hyperoxaluria (>40 mg/24 h) received daily a mixture containing 8 x 10(11) freeze-dried lactic acid bacteria (L. acidophilus, L. plantarum, L. brevis, S. thermophilus, B. infantis) for four weeks. The 24-hour urinary excretion of oxalate was determined at the end of the study period and then one month after ending the treatment. The ability of bacteria to degrade oxalate and grow in oxalate-containing media, and the gene expression of Ox1T, an enzyme that catalyzes the transmembrane exchange of oxalate, also were investigated.. The treatment resulted in a great reduction of the 24-hour excretion of oxalate in all six patients enrolled. Mean levels +/- SD were 33.5 +/- 15.9 mg/24 h at the end of the study period and 28.3 +/- 14.6 mg/24 h one month after treatment was interrupted compared with baseline values of 55.5 +/- 19.6 mg/24 h (P < 0.05). The treatment was associated with a strong reduction of the fecal excretion of oxalate in the two patients tested. Two bacterial strains among those used for the treatment (L. acidophilus and S. thermophilus) proved in vitro to degrade oxalate effectively, but their growth was somewhat inhibited by oxalate. One strain (B. infantis) showed a quite good degrading activity and grew rapidly in the oxalate-containing medium. L. plantarum and L. brevis showed a modest ability to degrade oxalate even though they grew significantly in oxalate-containing medium. No strain expressed the Ox1T gene.. The urinary excretion of oxalate, a major risk factor for renal stone formation and growth in patients with idiopathic calcium-oxalate urolithiasis, can be greatly reduced with treatment using a high concentration of freeze-dried lactic acid bacteria. We postulate that the biological manipulation of the endogenous digestive microflora can be a novel approach for the prevention of urinary stone formation.

Topics: Adolescent; Adult; Bacteria; Bifidobacterium; DNA, Bacterial; Feces; Freeze Drying; Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Lactic Acid; Lactobacillus; Middle Aged; Oxalates; Oxalic Acid; Pilot Projects; Polymerase Chain Reaction; Streptococcus

Although frequently observed, the etiology of idiopathic hypercalciuria (IHC) remains largely unknown. A common hypothesis postulates intestinal hyperabsorption and/or a primary renal leak as the pathophysiological basis. The aim of our study was to investigate the regulation pattern of calcium homeostasis in patients with IHC by using a prolonged period of calcium restriction.. Twenty-seven patients with IHC were investigated. After a 3-week run-in period (dietary calcium content 700-1,000 mg/24 h), a standard calcium reduced diet (300 mg/24 h) was given for 4 weeks. Thereafter, the participants received again a normal calcium-containing diet. Values for urinary calcium, PTH and calcitriol levels of all participants were obtained at different phases of the study. Forty-three healthy persons served as controls.. During calcium restriction, two distinct groups were identified. One group displayed an increase (n = 12) in urinary calcium excretion, the second (n = 15) a marked reduction, respectively. In both groups, the values during calcium restriction were significantly different from baseline (p < 0.01). In the first group, the increase of urinary calcium excretion was accompanied by an increase of PTH and calcitriol. These values were also significantly different from baseline values (p < 0.01). The control group showed decreasing calcium excretion during oral restriction (p < 0.01).. Prolonged calcium restriction proved to be useful in distinguishing apparently two major forms of IHC. The fact that one group displayed the same excretion pattern as the control group raises the question if this group just represents the upper limit of a physiological range. These findings may shed new light on diagnosis, pathogenesis and treatment of patients with IHC.

Topics: Calcitriol; Calcium; Calcium, Dietary; Child; Child, Preschool; Diagnosis, Differential; Diet; Female; Humans; Hyperparathyroidism, Secondary; Kidney Calculi; Male; Oxalates; Parathyroid Hormone; Prospective Studies; Sodium; Uric Acid

The purpose of this article is to evaluate the impact of low protein and high fiber intakes on risk factors of stone recurrence in idiopathic calcium stone formers (ICSFs).. Ninety-six ICSFs were randomly assigned a low animal protein diet (< 10% of total energy), a high-fiber diet (> 25 g/day), or a usual diet (control group); all patients were recommended to increase their fluid intake. Their daily urine compositions were analyzed at baseline and at four months. Compliance with dietary recommendations was checked by validated food frequency questionnaires. Compliance with total and animal protein intakes was assessed by 24-hour urea and sulfate outputs, respectively. The nutritional intervention (oral instructions, written leaflet, phoning) and food assessment were carried out by a research dietitian.. At baseline, diets and the daily urine composition did not differ between the three groups. At four months, while diets differed significantly, the 24-hour output of calcium and oxalate did not differ significantly within and between groups after adjustment for potential confounders (age, sex, and personal and family history of calcium stones) and baseline values. However, as many as 12 out of 31 ICSFs (95% CI, 22 to 58%) assigned to a low animal protein diet achieved a reduction in the urine urea excretion rate of more than 50 mmol/day and also exhibited a significant decrease in urinary calcium excretion that averaged 1.8 mmol/day. A significant correlation between urea and calcium outputs was observed only among patients with hypercalciuria.. These results show that only ICSFs who markedly decrease their animal protein intake, especially those with hypercalciuria, can expect to benefit from dietary recommendations.

Topics: Adult; Animals; Calcium; Dietary Fiber; Dietary Proteins; Female; Humans; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates; Recurrence; Risk Factors; Time Factors; Urine

The determinations of oxalate in urine and plasma are important in the evaluation and treatment of patients with calcium oxalate nephrolithiasis. Although many analytical methods for determining oxalate have been developed, most of them need complicated sample preparation, and are expensive for routine examination. Especially for estimation of plasma oxalate, much more sensitive measurement is required because of the extremely low concentration. A simple and rapid assay for oxalate in urine and plasma by capillary electrophoresis has been described here, and utilized for assessment of renal oxalate clearance. In addition, simultaneous determination of urinary oxalate and citrate was developed.. A Waters Quanta 4000E system was used with a detection at 185 nm. Separation was obtained on a fused silica capillary, 60 cm long x 75 microns and 100 microns (i.d.) for urine and plasma samples respectively. Urine samples were diluted with 60 mM hydrochloric acid, and ultrafiltrates of plasma were acidified and diluted with 300 mM boric acid and 50 mM phosphoric acid.. The intraassay coefficient variation was 2.7-4.0% for urinary oxalate, and 1.3-3.9% for citrate. The mean recovery ratio of 0.2 mM oxalate and 1.0 mM citrate added to 10 samples were 99.0% (92.6-107.4%) and 98.4% (91.2-103.9%), respectively. In the determination of plasma oxalate, the minimum detectable limit was 0.9 microM, the coefficient variation was 5.8-16.0%, and the recovery rate was 101.5% (87.8-125.6%). The plasma oxalate levels in 8 adult males were 2.39 +/- 1.46 microM (Mean +/- SD). Renal oxalate clearances with one hour method were 72.9 +/- 20.0 ml/min in 6 healthy controls and 83.2 +/- 27.8 ml/min in 8 stone formers. Oxalate/creatinine clearance ratios in each groups were 0.70 +/- 0.16 and 1.11 +/- 0.34 respectively.. The simultaneous determination of urinary oxalate and citrate was satisfactory. Capillary electrophoresis is suited for routine examination of urinary oxalate and citrate with the advantage on simplicity and economy. The assay of plasma oxalate by this method was also acceptably sensitive, specific under a low temperature and an acidification.

Topics: Adult; Biomarkers; Calcium Oxalate; Citrates; Electrophoresis, Capillary; Female; Humans; Kidney Calculi; Male; Metabolic Clearance Rate; Oxalates; Reproducibility of Results; Sensitivity and Specificity

While there is general agreement on the need to increase urinary volume in stone formers, contrasting opinions have been expressed about the hardness of water and stone incidence. We evaluate the influence of 3 types of mineral water on urinary analytes in 22 idiopathic calcium oxalate stone formers.. All patients underwent a nutritional and metabolic evaluation at baseline, and after a controlled diet including water with a high, medium or low calcium content.. In patients who drank water with high and medium calcium contents calcium excretion increased, although the results did not reach statistical significance. In those who drank water with the highest calcium content oxalate excretion significantly decreased (p = 0.05), as did the oxalate-to-calcium ratio (p = 0.05). Moreover, these modifications did not induce relevant changes in urinary saturation. In patients who drank water with the greatest amount of bicarbonate citrate excretion increased (p = 0.03).. Mineral water with a higher calcium content induced increased calcium excretion but significantly decreased oxalate excretion. These data are in accordance with those of others, who did not find definite evidence that hard water is more lithogenic than soft water. Furthermore, water components other than calcium can modify the tendency toward crystal formation, affecting inhibitory power and/or lithogenic salt excretion.

Topics: Adult; Calcium; Female; Humans; Kidney Calculi; Male; Middle Aged; Mineral Waters; Oxalates; Risk Factors

Increasing intake of dietary calcium from less than 400 mg to 800 mg daily may decrease the absorption of dietary oxalate, which in turn would decrease urinary oxalate excretion. The effect of substituting milk for apple juice on urine composition and risk of calcium oxalate precipitability was studied.. Twenty-one normocalciuric adults with a history of at least 1 calcium oxalate stone and urinary oxalate excretion exceeding 275 micromol/day on their self-selected diet.. Randomized crossover trial.. Each participant consumed two moderate-oxalate (2,011 micromol/day) study diets, which were identical except that one contained 360 mL milk and the other contained 540 mL apple juice as the beverage with meals.. Four days free-living then 2 days in the metabolic unit of a university nutrition department.. Tiselius risk index for calcium oxalate precipitability calculated from urine composition.. Paired t tests.. Twenty-four hour urinary oxalate excretion was 18% lower (P<.0001) on the milk diet vs the juice diet: 423 vs 514 micromol, respectively. Calcium excretion was 17% higher (P<.05) on the milk vs juice diet: 4.7 vs 3.9 mmol, respectively. Urinary magnesium and citrate excretion, volume, and Tiselius risk index did not differ between diets.. Substituting 360 mL milk daily for apple juice with meals in a diet containing moderate amounts of dietary oxalate from whole grains, legumes, fruits, and vegetables does not increase the risk index of calcium oxalate precipitability in most normocalciuric adults who form stones.

Topics: Adult; Aged; Animals; Beverages; Calcium; Calcium Oxalate; Calcium, Dietary; Cross-Over Studies; Female; Humans; Kidney Calculi; Male; Middle Aged; Milk; Oxalates; Risk Factors; Rosales

This study was undertaken to identify a South African mineral water containing relatively high concentrations of calcium and magnesium and to investigate its effect on urinary biochemical and physicochemical risk factors associated with calcium oxalate kidney stone formation.. The study followed a change-over design in which each subject followed a randomised sequence of three water-drinking protocols involving their normal diet, a calcium and magnesium-rich mineral water and a mineral water deficient in these elements.. University of Cape Town.. 54 volunteers without any previous history of stone disease (27 men, 27 women) in the age group 21-35 years and 31 with a history of calcium oxalate kidney stones (24 men, 7 women) in the age group 25-45 years participated in the study.. Both mineral waters favourably altered several risk factors. However, the effect of the calcium- and magnesium-rich water was shown to be significantly greater as it altered a larger number of these factors and induced several unique changes that were not achieved by the other water.. The risk of calcium oxalate stone formation can be significantly reduced by consumption of mineral water which is rich in calcium and magnesium.

Topics: Adult; Calcium; Calcium Oxalate; Case-Control Studies; Cross-Over Studies; Crystallization; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Mineral Waters; Oxalates; Risk Factors; South Africa

Urolithiasis is a very frequent finding in the Sudan, but stone analysis is not routinely performed in this country. It would, however, give important evidence for the metabolic basis of stone formation. We therefore set out to analyze urinary stones in 80 Sudanese patients (45 male, 35 female), 12 of whom where children. Fourier-transformed infrared spectroscopy was used for stone analysis. As is known from other countries, calcium oxalate (CaOx) stones were the most frequent, with 68.7% of all stones in adults and 43.7% of childhood stones. Uric acid and uric acid dihydrate stones were more often seen in adults (13.2%) than in children (4. 1%). Ammonium urate stones are common in the Sudan, especially in children (32.9%), which is typical for underdeveloped countries. Infectious stones (struvite and carbonate apatite) were more often found in women (7.0%) and in children (5.3%) than in men (1.4%). Brushite stones were seldom seen and cystine stones did not occur.

Topics: Adolescent; Adult; Calcium Oxalate; Child; Child, Preschool; Female; Humans; Incidence; Kidney Calculi; Male; Middle Aged; Oxalates; Spectrophotometry; Sudan; Uric Acid

We have established normal values for calcium/creatinine (Ca/Cr) and oxalate/creatinine (Ox/Cr) ratios in 25 infants (aged 1-7 days) and 391 children (aged 1 month to 14.5 years) and compared these with values obtained in 137 children with post-glomerular haematuria and 27 with nephrolithiasis. Oxalate was measured by ion chromatography. Nomograms of Marshall and Robertson were used to calculate urine saturation to calcium oxalate. The Ca/Cr ratio was normally distributed whereas the Ox/Cr ratio had a log-normal distribution. The molar ratio of Ca/Cr was the lowest in the first days of life and the highest between 7 month and 1.5 years (mean +/- SD = 0.39 +/- 0.28 mmol/mmol). Following a slight decrease it stabilised by the age of 6 years (0.34 +/- 0.19 mmol/mmol). The highest Ox/Cr values were measured during the 1st month of life [geometric mean 133 (range 61-280) mumol/mmol], followed by a gradual decrease until 11 years of age [mean 24 (range 6-82) mumol/mmol]. Thirty-six haematuric children had hypercalciuria (26%), 23 had absorptive hypercalciuria, 13 renal type. Children with absorptive hypercalciuria on a calcium-restricted diet had significantly higher oxalate excretion than those with renal hypercalciuria and the control group [38 (range 28-49) vs. 22 (range 16-29) and 23 (range 22-27) mumol/mol respectively, P < 0.01]. Calcium oxalate urine saturation of stone patients was higher than that of patients with haematuria and the normal population (1.18 +/- 0.05 vs. 1.06 +/- 0.03, P < 0.03 and 0.84 +/- 0.03, P < 0.001 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Aging; Calcium; Child; Child, Preschool; Chromatography, Ion Exchange; Creatinine; Female; Hematuria; Humans; Infant; Infant, Newborn; Kidney Calculi; Male; Oxalates; Reference Values; Water-Electrolyte Balance

An anomaly in erythrocyte oxalate transport has been reported in patients with idiopathic calcium oxalate nephrolithiasis. Even if clinical and experimental evidence suggests a causal role of this cellular anomaly in calcium nephrolithiasis, a definitive answer to this fundamental question is still lacking. We approached this problem by searching for a possible relationship between the erythrocyte oxalate self-exchange anomaly and the renal clearance of this anion in stone formers. In 10 idiopathic calcium-oxalate renal stone formers, and 10 healthy subjects we evaluated the erythrocyte oxalate flux rate, and the renal fractional clearance of oxalate by a recently described enzymathic procedures for plasma oxalate determination. With respect to controls, stone formers had higher oxalate flux rate in erythrocytes, and higher oxalate renal fractional clearance with a significant direct correlation between the two parameters. These data are compatible with a membrane transport abnormality within the kidney of these stone formers, and the existence of a common defect of the oxalate transport shared by both erythrocytes and tubular renal cells. The latter may be crucial in the pathogenesis of calcium oxalate nephrolithiasis, by modifying the renal handling of oxalate.

Topics: Adult; Calcium; Erythrocyte Membrane; Female; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Oxalates

We examined the biochemical changes and the efficacy of indapamide in the prevention of calcium stone recurrences. Seventy-five patients with calcium nephrolithiasis and hypercalciuria were randomly assigned to three different therapies: diet and fluid (group A), diet and fluid plus indapamide 2.5 mg/day (group B), and diet and fluid plus indapamide 2.5 mg/day plus allopurinol 300 mg/day (group C). Before treatment and after 6, 12, 24, and 36 months of therapy, we evaluated blood pressure, serum and urine risk parameters (including relative supersaturations of calcium oxalate, calcium phosphate and uric acid), stone rate, and the proportion of calculi-free patients. During the 3 years of treatment, urinary calcium greatly decreased in groups B and C, dropping to 50% of the pretreatment values; urinary oxalate also significantly declined in group B (-24%) and group C (-27%). Relative supersaturations of calcium oxalate and calcium phosphate decreased to the same extent in groups B and C (about one-half of the pretreatment value), and relative supersaturation of uric acid was particularly reduced in group C (-65% of the pretreatment value). The stone rate improved in all three groups (p < 0.005), but using actuarial analysis in the evaluation of calculi-free patients, indapamide, and indapamide plus allopurinol groups were found to have a significantly more favorable effect than diet and fluid treatment (p < 0.02), without any difference between the two drug groups. Because indapamide has fewer side effects than thiazide diuretics, we conclude that indapamide could be an interesting alternative to thiazides in the prevention of calcium stones in hypercalciuric patients.

Topics: Adult; Allopurinol; Blood Chemical Analysis; Blood Pressure; Calcium; Female; Follow-Up Studies; Heart Rate; Humans; Indapamide; Kidney Calculi; Male; Middle Aged; Oxalates; Prospective Studies; Recurrence

An organic marine hydrocolloid (OMH) charged with calcium ('Ox-Absorb') was studied in vitro for oxalate binding and in patients with enteric hyperoxaluria to investigate oxalate excretion and the inhibitory activity on crystal formation of the urine. In-vitro experiments showed complete binding of oxalate to OMH. In clinical studies in nineteen patients with intestinal disorders and stone formation, urinary oxalate excretion was significantly lower during OMH treatment than off treatment. The activity product index of calcium oxalate was reduced on treatment. A pronounced rise in the inhibitory activity of urine was seen in two patients with very low pretreatment values. Most patients experienced virtual normalisation of bowel function, and in those with severe stone formation there was substantial clinical improvement. It is concluded that OMH has the capacity to bind oxalate in vitro and to reduce urinary oxalate excretion. These observations suggest a new promising treatment for enteric hyperoxaluria.

Topics: Administration, Oral; Adult; Calcium; Clinical Trials as Topic; Colloids; Drug Evaluation; Female; Humans; Hyperoxaluria; Intestinal Absorption; Intestinal Diseases; Intestine, Small; Kidney Calculi; Male; Middle Aged; Oxalates; Pilot Projects; Postoperative Complications; Recurrence; Tablets; Time Factors; Zinc

17 cystine stone patients were treated with high doses of ascorbic acid (5 g p. d.). During the observation period, a total of only two natural passages of cystine stones could be observed. For five patients the therapeutic strategy was altered because the recurrence rate did not change and the cystine concentration in the urine was enhanced. One mixed calcium-oxalate/cystine stone had to be resected. In this case as well as on the occasion of further medical check-ups of other patients, an increased risk of calcium-oxalate stone formation was signalled by an enhanced oxalic-acid concentration in the 24-hour urine. Changes in blood serum and impairment in hepatic and renal functions were not observed. With three patients, the therapy had to be interrupted because of gastritis symptoms. The use of high-dose ascorbic acid therapy is recommended and is continued. In special cases, an additive of low do ses of alpha-mercaptopropionyl-glycine is recommended.

Topics: Adult; Aged; Ascorbic Acid; Child; Clinical Trials as Topic; Cystinuria; Disease Susceptibility; Dose-Response Relationship, Drug; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Long-Term Care; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence

Topics: Calcium; Citrates; Clinical Trials as Topic; Cystine; Cystinuria; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Oxalic Acid; Uric Acid

Topics: Adult; Calcium; Clinical Trials as Topic; Female; Humans; Ileum; Intestinal Absorption; Jejunum; Kidney Calculi; Male; Middle Aged; Obesity; Oxalates; Surgical Procedures, Operative

In patients with urolithiasis "Nephrolith" has a favourable influence on many parameters which are responsible for the development of renal calculi. I could never observe a complete dissolution of the urinary calculi.

Topics: Adolescent; Adult; Aged; Bacterial Infections; Calcium; Child; Child, Preschool; Clinical Trials as Topic; Drug Combinations; Drug Evaluation; Female; Humans; Khellin; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Sulfonamides; Urinary Calculi

Quantitative and qualitative studies have been made of the urinary crystals from a series of normal subjects and from stone formers with idiopathic hypercalciuria with and without treatment with thiazide diuretics and/or cellulose phosphate. The results obtained from mid-morning unprepared subjects seemed more helpful than those obtained following overnight collections or after a dry breakfast. Crystalluria was more common in stone formers than in normal subjects, but was seen in both groups. The most striking difference between these 2 groups was the almost complete absence of aggregation of oxalate crystals in the normal subjects. Cellulose phosphate greatly reduced phosphate crystals but resulted in a large increase in small oxalate crystals but without change in the incidence of aggregation of oxalate crystals. Thiazides also reduced occurrence of phosphate crystals but only gave a very small increase in oxalate crystals and also without change in aggregation of oxalate crystals.

Topics: Adult; Benzothiadiazines; Calcium; Calcium Phosphates; Cellulose; Clinical Trials as Topic; Crystallization; Diuretics; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Phosphates; Sodium Chloride Symporter Inhibitors

Topics: Clinical Trials as Topic; Glycols; Glyoxylates; Humans; Kidney; Kidney Calculi; Oxalates; Oxygen Consumption; Succinates; Succinimides

Topics: Adolescent; Adult; Calcium; Child; Clinical Trials as Topic; Crystallization; Humans; Kidney Calculi; Methods; Oxalates; Staining and Labeling; Urinary Bladder Calculi

Topics: Calcium; Calcium Phosphates; Clinical Trials as Topic; Humans; Kidney Calculi; Magnesium; Microscopy, Polarization; Minerals; Oxalates; Phosphates; Uric Acid

Primary hyperoxaluria type 1 (PH1) is a rare, severe genetic disease causing increased hepatic oxalate production resulting in urinary stone disease, nephrocalcinosis, and often progressive chronic kidney disease. Little is known about the natural history of urine and plasma oxalate values over time in children with PH1.. For this retrospective observational study, we analyzed data from genetically confirmed PH1 patients enrolled in the Rare Kidney Stone Consortium PH Registry between 2003 and 2018 who had at least 2 measurements before age 18 years of urine oxalate-to-creatinine ratio (Uox:cr), 24-h urine oxalate excretion normalized to body surface area (24-h Uox), or plasma oxalate concentration (Pox). We compared values among 3 groups: homozygous G170R, heterozygous G170R, and non-G170R AGXT variants both before and after initiating pyridoxine (B6).. Of 403 patients with PH1 in the registry, 83 met the inclusion criteria. Uox:cr decreased rapidly over the first 5 years of life. Both before and after B6 initiation, patients with non-G170R had the highest Uox:cr, 24-h Uox, and Pox. Patients with heterozygous G170R had similar Uox:cr to homozygous G170R prior to B6. Patients with homozygous G170R had the lowest 24-h Uox and Uox:cr after B6. Urinary oxalate excretion and Pox tend to decrease over time during childhood. eGFR over time was not different among groups.. Children with PH1 under 5 years old have relatively higher urinary oxalate excretion which may put them at greater risk for nephrocalcinosis and kidney failure than older PH1 patients. Those with homozygous G170R variants may have milder disease. A higher resolution version of the Graphical abstract is available as Supplementary information.

Topics: Adolescent; Child; Child, Preschool; Humans; Hyperoxaluria, Primary; Kidney Calculi; Nephrocalcinosis; Oxalates

Injury to the renal tubular epithelium has emerged as a leading factor underlying the formation of kidney stones. Indeed, epithelial cell damage contributes to the adherence and aggregation of crystals, thereby accelerating the formation of renal stones. Meanwhile, exosomes play an instrumental role in cellular communication, including DNA, RNA, mRNA, etc. In this study, homogenous cells were treated with exosomes derived from damaged cells in an attempt to establish "positive feedback" of cell damage, and the desired results were achieved. To begin, a serum-free medium and supersaturated concentrations of oxalate were added to the HK-2 cell line, and then exosomes were isolated from the two groups for analysis and comparison, and the autophagy-related gene Ambra1 (autophagy and beclin-1 regulator 1) was detected. Subsequently, normal HK-2 cells were treated with exosomes, and the related indexes of autophagy, ferroptosis and mitophagy were determined. Thereafter, Ambra1 was knocked down in exosome-derived HK-2 cells, resulting in the down-regulation of Ambra1 expression in exosomes produced by HK-2 cells following oxalate intervention. Thereafter, the ability of exosomes to stimulate autophagy, mitophagy and ferroptosis was re-evaluated in HK-2 cells after Ambra1 knockdown. The results corroborated that exosomes secreted by oxalate-treated HK-2 can directly elevate autophagy, ferroptosis and mitophagy levels in normal cells, and this effect was significantly mitigated following Ambra1 knockdown within exosomes. Meanwhile, exosomes-induced autophagy and ferroptosis were alleviated after knockdown of beclin-1 in recipient HK-2 cells. These results further suggest that beclin-1 plays a critical role in the process of exosome-induced autophagy-ferroptosis.

Topics: Autophagy; Beclin-1; Cell Line; Exosomes; Ferroptosis; Humans; Kidney Calculi; Mitophagy; Oxalates

Knowledge of kidney stone composition can help in patient management; urine composition analysis and dual-energy CT are frequently used to assess stone type. We assessed if threshold-based stone segmentation and radiomics can determine the composition of kidney stones from single-energy, non-contrast abdomen-pelvis CT.. With IRB approval, we identified 218 consecutive patients (mean age 64 ± 13 years; male:female 138:80) with the presence of kidney stones on non-contrast, abdomen-pelvis CT and surgical or biochemical proof of their stone composition. CT examinations were performed on one of the seven multidetector-row scanners from four vendors (GE, Philips, Siemens, Toshiba). Deidentified CT images were processed with a radiomics prototype (Frontier, Siemens Healthineers) to segment the entire kidney volumes with an AI-based organ segmentation tool. We applied a threshold of 130 HU to isolate stones in the segmented kidneys and to estimate radiomics over the segmented stone volume. A coinvestigator verified kidney stone segmentation and adjusted the volume of interest to include the entire stone volume when necessary. We applied multiple logistic regression tests with precision recall plots to obtain area under the curve (AUC) using a built-in R statistical program.. The threshold-based stone segmentation successfully isolated kidney stones (uric acid: n = 102 patients, calcium oxalate/phosphate: n = 116 patients) in all patients. Radiomics differentiated between calcium and uric acid stones with an AUC of 0.78 (p < 0.01, 95% CI 0.73-0.83), 0.79 sensitivity, and 0.90 specificity regardless of CT vendors (GE CT: AUC = 0.82, p < 0.01, 95% CI 0.740-0896; Siemens CT: AUC = 0.77, 95% CI 0.700-0.846, p < 0.01).. Automated threshold-based stone segmentation and radiomics can differentiate between calcium oxalate/phosphate and urate stones from non-contrast, single-energy abdomen CT.

Topics: Aged; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Tomography, X-Ray Computed; Uric Acid

Roux-en-Y gastric bypass (RYGB) is associated with an increased risk of kidney stone formation. This is not observed after sleeve gastrectomy (SG).. Aim of this study was to assess whether preoperative metabolic profiling is helpful in selecting the most optimal bariatric procedure for patients with a kidney stone history.. General hospital, the Netherlands.. Patients with a kidney stone history and in the run up to bariatric surgery were screened with non-contrast abdominal computed tomography (CT), serum profiling, and 24-hour urine analysis. Those with stones on radiologic imaging and/or high preoperative urinary oxalate were advised to undergo SG instead of RYGB. Pre- and postoperative urine and serum profile differences between both groups were evaluated retrospectively.. Postoperatively, RYGB (N = 28, M:F = 8:20) was associated with a 23.5% reduction in urinary volume, a 85% increase in urinary oxalate excretion with a 230% increase in calcium oxalate (CaOx) supersaturation and a 62% decrease in urinary citrate. Although SG (N = 30, M:F = 12:18) was also associated with a reduction in urinary volume, it had no adverse effects on urinary oxalate and citrate excretion, nor on calcium oxalate supersaturation (CaOx-SS). Both RYGB and SG showed favorable effects on postoperative sodium, calcium, uric acid, and phosphate excretion.. This study indicates that preoperative metabolic profiling is important to select the optimal bariatric procedure in patients with an a priori increased risk of kidney stone development. These patients should be strongly encouraged to undergo SG instead of RYGB to prevent progressive or recurrent kidney stone disease.

Topics: Bariatric Surgery; Calcium Oxalate; Citric Acid; Gastrectomy; Gastric Bypass; Humans; Kidney Calculi; Obesity, Morbid; Oxalates; Retrospective Studies; Risk Factors

A microfluidic paper-based analytical device (μPAD) coupled with colorimetric detection was developed for simultaneous determination of urinary oxalate, citrate and uric acid (UA) which are important biomarkers of nephrolithiasis or kidney stones. The colorimetric detections were based on enzymatic reactions using oxalate oxidase and uricase for oxalate and UA, respectively, while an indicator displacement assay (IDA) using a copper murexide complex was applied for citrate detection. The developed μPAD was successfully applied for simultaneous determination of the three biomarkers in urine within 25 min, with linear ranges of 2-40, 5-150, and 5-45 mg L

Topics: Biomarkers; Citrates; Citric Acid; Colorimetry; Humans; Kidney Calculi; Microfluidics; Oxalates; Uric Acid

A high concentration of oxalate is associated with an increased risk of kidney calcium oxalate (CaOx) stones, and the degradation of exogenous oxalate mostly depends on oxalate-degrading enzymes from the intestinal microbiome. We found that zinc gluconate supplement to patients with CaOx kidney stones could significantly improve the abundance of oxalate metabolizing bacteria in humans through clinical experiments on patients also subjected to antibiotic treatment. The analysis of clinical samples revealed that an imbalance of Lactobacillus and oxalate decarboxylase (OxDC) was involved in the formation of CaOx kidney stones. Then, we identified that Zn

Topics: Animals; Calcium; Calcium Oxalate; Humans; Kidney Calculi; Lactobacillus; Oxalates; Rats; Zinc

The purpose of this paper is to help patients with calcium oxalate stones to access prevention and treatment options with dietary management.. Typical cases in our hospital and other hospitals were selected for case review; combined with literature review through PubMed search, comprehensive analysis and suggestions were put forward.. By retrieving the literature with sufficient evidence, selecting, and summarizing, analysis of dietary liquid, oxalate and oxalate precursors, calcium, protein, fruits and vegetables, salt, high dietary fiber, and other content with high evidence index was carried out, respectively.. Through the retrospective analysis of typical cases and literature review, the importance of diet management in the prevention and treatment of calcium oxalate stones was emphasized again, and suggestions were put forward to promote the prevention and treatment of calcium oxalate stones.

Topics: Calcium; Calcium Oxalate; Humans; Kidney Calculi; Oxalates; Retrospective Studies

Nephrolithiasis is a common disease that seriously affects the health and life quality of patients. Despite the reported effect of hyperoside (Hyp) against nephrolithiasis, the specific mechanism has not been clarified. Therefore, this study is aimed at investigating the effect and potential mechanism of Hyp on renal injury and calcium oxalate (CaOx) crystal deposition.. Rat and cell models of renal calculi were constructed by ethylene glycol (EG) and CaOx induction, respectively. The renal histopathological damage, CaOx crystal deposition, and renal function damage of rats were assessed by HE staining, Pizzolato staining, and biochemical detection of blood and urine parameters. MTT and crystal-cell adhesion assays were utilized to determine the activity of HK-2 cells and crystal adhesion ability, biochemical detection and enzyme-linked immunosorbent assay (ELISA) to measure the levels of oxidative stress-related substances and inflammatory factors, and western blot to test the expression levels of proteins related to the AMPK/Nrf2 signaling pathway.. Hyp can improve renal pathological and functional damage, decrease CaOx crystal deposition, and inhibit oxidative stress and inflammatory response. Such effects may be achieved by activating the AMPK/Nrf2 signaling pathway.

Topics: AMP-Activated Protein Kinases; Animals; Calcinosis; Calcium Oxalate; Kidney; Kidney Calculi; NF-E2-Related Factor 2; Oxalates; Oxidative Stress; Rats; Signal Transduction

To analyze the dose-dependent preventive effect of a plant-based herbal product on the new crystal formation in a rat model.. A total of 42 rats were divided into 7 groups and zinc discs were placed into the bladder of rats to provide a nidus for the development of new crystal formation: Group 1: control, Group 2: 0.75 percent ethylene glycol (EG); Group 3: 0.75 percent EG plus 0.051 ml of the compound; Group 4: 0.75 percent EG plus 0.179 ml of the compound; Group 5: 0.75 percent EG plus 0.217 ml of the compound; Group 6: 0.75 percent EG plus 0.255 ml of the compound; Group 7 0.75 percent EG plus 0.332 of the compound). The analysis and comparison focused on the disc weights, changes in urinary oxalate and calcium levels, urinary pH, and the histopathologic evaluation of the inflammatory changes in the bladder after 14 days.. According to the evaluation of discs placed in the bladders of the animals, animals receiving the herbal compound on a dose-dependent basis showed a limited increase in the disc weights values after 14 days, despite a considerable increase in animals receiving EG alone (p = 0.001). Further evaluation of the increase in disc weights on a dose-dependent basis in different subgroups (from Groups 3 to 7) demonstrated that the limitation of crystal deposition began to be more prominent as the dose of herbal compound increased. This effect was more evident particularly in comparisons between group 7 and others, according to LSD multiple comparison tests (p = 0.001). As anticipated, there has been no discernible change in the weight of the discs in the control group. Although urinary calcium levels in animals of Groups 2, 6, and 7 were significantly higher than the other groups, we were not able to demonstrate a close correlation between urinary oxalate levels and the increasing dose levels. Even though mean urine pH levels were statistically considerably higher in Group 3, there was no statistically significant correlation between the oxalate and calcium levels between all groups, and no association was seen with the administration of herbal agents. The transitional epithelium between the three groups of animals' bladder samples did not exhibit any appreciable difference according to pathological analysis.. In this animal model, the treatment of the compound was successful in lowering the amount of crystal deposition surrounding the zinc discs, most noticeably at a dosage of 0.332 ml, three times per day.

Topics: Animals; Calcium; Calcium Oxalate; Drugs, Chinese Herbal; Kidney; Kidney Calculi; Oxalates; Rats; Urinary Bladder; Zinc

Kidney stones (KSs) are very common, excruciating, and associated with tremendous healthcare cost, chronic kidney disease (CKD), and kidney failure (KF). Most KSs are composed of calcium oxalate and small increases in urinary oxalate concentration significantly enhance the stone risk. Oxalate also potentially contributes to CKD progression, kidney disease-associated cardiovascular diseases, and poor renal allograft survival. This emphasizes the urgent need for plasma and urinary oxalate lowering therapies, which can be achieved by enhancing enteric oxalate secretion. We previously identified

Topics: Animals; Caco-2 Cells; Epithelial Cells; Humans; Hyperoxaluria; Kidney Calculi; Kidney Transplantation; Mice; Oxalates; Oxalobacter formigenes; Peptides; Renal Insufficiency; Renal Insufficiency, Chronic

A probiotic is a living microorganism that promotes host health when grown under appropriate conditions. Kidney stones are one of the universal agonizing diseases that have increased dramatically in recent years. One of the causes of this disease is hyperoxaluria (HOU), which is known to be an important factor in the formation of oxalate stones and is manifested by high levels of oxalate in the urine. In addition, about 80% of kidney stones contain oxalate, and decomposition of this material by microbes is one way to dispose of it.. Therefore, we examined a bacterial mixture containing Lactobacillus plantarum, Lactobacillus casei, Lactobacillus acidophilus, and Bifidobacterium longum to prevent of oxalate production in Wistar rats with kidney stones. We divided the rats into 6 groups defined in the method.. The results of this study clearly show a decrease in urinary oxalate levels by exogenous means by L. plantarum, L. casei, L. acidophilus, and B. longum at the beginning of the experiment. Therefore, these bacteria can be used to control and prevent the formation of kidney stones.. However, further studies should be conducted on the effects of these bacteria, and it is recommended to identify the gene responsible for the degradation of oxalate in order to develop a new probiotic.

Topics: Animals; Bacteria; Bifidobacterium; Kidney Calculi; Lactobacillus; Oxalates; Rats; Rats, Wistar

The global prevalence of pediatric nephrolithiasis continues to rise amidst increased sodium and animal protein intake. Plant-based meat alternatives (PBMAs) have recently gained popularity due to health benefits, environmental sustainability, and increased retail availability. PBMAs have the potential to reduce the adverse metabolic impact of animal protein on kidney stone formation. We analyzed PBMAs targeted to children to characterize potential lithogenic risk vs animal protein.. We performed a dietary assessment using a sample of PBMAs marketed to or commonly consumed by children and commercially available at national retailers. Nutrient profiles for PBMAs were compiled from US Department of Agriculture databases and compared to animal protein sources using standardized serving sizes. We also analyzed nutrient profiles for plant-based infant formulas against typical dairy protein-based formulas. Primary protein sources were identified using verified ingredient lists. Oxalate content was extrapolated from dietary data sources.. A total of 41 PBMAs were analyzed: chicken (N = 18), hot dogs (N = 3), meatballs (N = 5), fish (N = 10), and infant formula (N = 5). Most products (76%) contained a high-oxalate ingredient as the primary protein source (soy, wheat, or almond). Average oxalate content per serving was substantially higher in these products (soy 11.6 mg, wheat 3.8 mg, almond 10.2 mg) vs animal protein (negligible oxalate). PBMAs containing pea protein (24%) had lower average oxalate (0.11 mg). Most PBMAs averaged up to six times more calcium and three times more sodium per serving compared to their respective animal proteins. Protein content was similar for most categories.. Three-quarters of the examined plant-based meat products for children and infants contain high-oxalate protein sources. Coupled with higher per-serving sodium and calcium amounts, our findings raise questions about possible lithogenic risk in some PBMAs, and further studies are needed to assess the relationship between PBMAs and nephrolithiasis.

Topics: Animals; Calcium; Calcium, Dietary; Child; Humans; Infant; Kidney Calculi; Meat; Oxalates; Risk Factors; Sodium

Calcium oxalate (CaOx) stones are among the most common types of kidney stones and are associated with renal tubular damage, interstitial fibrosis, and chronic kidney disease. The mechanism of CaOx crystal-induced renal fibrosis remains unknown. Ferroptosis, a type of regulated cell death, is characterised by iron-dependent lipid peroxidation, and the tumour suppressor p53 is a key regulator of ferroptosis. In the present study, our results demonstrated that ferroptosis was significantly activated in patients with nephrolithiasis and hyperoxaluric mice as well as verified the protective effects of ferroptosis inhibition on CaOx crystal-induced renal fibrosis. Moreover, the single-cell sequencing database, RNA-sequencing, and western blot analysis revealed that the expression of p53 was increased in patients with chronic kidney disease and the oxalate-stimulated human renal tubular epithelial cell line, HK-2. Additionally, the acetylation of p53 was enhanced by oxalate stimulation in HK-2 cells. Mechanistically, we found that the induction of p53 deacetylation, owing to either the SRT1720-induced activation of deacetylase sirtuin 1 or the triple mutation of p53, inhibited ferroptosis and alleviated renal fibrosis caused by CaOx crystals. We conclude that ferroptosis is one of the critical mechanisms contributing to CaOx crystal-induced renal fibrosis, and the pharmacological induction of ferroptosis via sirtuin 1-mediated p53 deacetylation may be a potential target for preventing renal fibrosis in patients with nephrolithiasis.

Topics: Animals; Calcinosis; Calcium Oxalate; Ferroptosis; Fibrosis; Humans; Kidney; Kidney Calculi; Mice; Oxalates; Renal Insufficiency, Chronic; Sirtuin 1; Tumor Suppressor Protein p53

High oxalate level in blood and urine may cause oxalate-related disorders, particularly kidney stone disease. To unravel disease mechanisms, investigations of oxalate level and its binding proteins are required. However, the information on oxalate-binding proteins is limited due to a lack of appropriate tool for their investigations. Therefore, we have developed a freely accessible web-based tool, namely OxaBIND (https://www.stonemod.org/oxabind.php), to identify oxalate-binding site(s) in any proteins of interest. The prediction model was generated by recruiting all of the known oxalate-binding proteins with solid experimental evidence (from PubMed and RCSB Protein Data Bank). The potential oxalate-binding domains/motifs were predicted from these oxalate-binding proteins using PRATT tool and used to discriminate these known oxalate-binding proteins from the known non-oxalate-binding proteins. The best one, which provided highest fitness score, sensitivity and specificity, was then implemented to create the OxaBIND tool. After inputting protein identifier or sequence (which can be single or multiple), details of all the identified oxalate-binding site(s), if any, are presented in both textual and graphical formats. OxaBIND also provides theoretical three-dimensional (3D) structure of the protein with oxalate-binding site(s) being highlighted. This tool will be beneficial for future research on the oxalate-binding proteins, which play important roles in the oxalate-related disorders.

Topics: Binding Sites; Carrier Proteins; Humans; Kidney Calculi; Oxalates; Proteins

Primary hyperoxaluria is a genetic disorder of the metabolism of glyoxylate, the precursor of oxalate. It is characterized by high endogenous production and excessive urinary excretion of oxalate, resulting in the development of calcium oxalate nephrolithiasis, nephrocalcinosis, and, in severe cases, end-stage kidney disease and systemic oxalosis. Three different forms of primary hyperoxaluria are currently known, each characterized by a specific enzymatic defect: type 1 (PH1), type 2 (PH2), and type 3 (PH3). According to currently available epidemiological data, PH1 is by far the most common form (about 80% of cases), and is caused by a deficiency of the hepatic enzyme alanine:glyoxylate aminotransferase.. A survey on rare forms of nephrolithiasis and nephrocalcinosis with a focus on primary hyperoxaluria in the setting of Italian Nephrology and Dialysis Centers, using an online questionnaire, was recently conducted by the Project Group "Rare Forms of Nephrolithiasis and Nephrocalcinosis" of the Italian Society of Nephrology, with the aim of assessing the impact and management of this disorder in clinical practice in Italy.. Forty-five public and private Italian Centers participated in the survey, and responses to the questionnaire were provided by 54 medical professionals. The survey results indicate that 21 out of the 45 participating Centers are managing or have managed primary hyperoxaluria patients, most of whom are on dialysis, or are recipients of kidney transplants.. The data of this survey indicate the need to implement genetic testing in suspected cases of primary hyperoxaluria, not only in the setting of dialysis or transplantation, but also with the aim of encouraging early diagnosis of PH1, which is the only type of primary hyperoxaluria for which specific drug therapy is currently available.

Topics: Humans; Hyperoxaluria, Primary; Kidney Calculi; Nephrocalcinosis; Nephrologists; Nephrology; Oxalates

Topics: Calcium; Calcium Oxalate; Diet; Humans; Hypercalciuria; Kidney Calculi; Oxalates

Primary hyperoxaluria (PH) is a rare genetic disorder characterized by the excessive production and accumulation of oxalate. We present five cases of PH, each exhibiting varying manifestations of the disorder including a case presenting as postpartum kidney failure. Notably, three of these cases involve a previously unreported mutation.. We evaluated five Indian patients who presented with varying manifestations of PH. The first case, a 30 year old woman, presented as post-partum kidney failure and was found to be having oxalate nephropathy precipitated by dietary oxalate overload in the setting of previously undiagnosed PH. Genetic analysis revealed a previously unreported mutation in the alanine-glyoxylate aminotransferase gene. The patient underwent simultaneous kidney liver transplant. The second and third cases, 26 and 28 year old women respectively, were asymptomatic siblings of the first patient, who were diagnosed through screening. The fourth case is a 12 year boy with PH type 1 presenting as nephrolithiasis and rapidly worsening kidney function requiring combined kidney liver kidney transplant. Case 5 is a 6 year old male child with type 2 PH presenting with nephrolithiasis, nephrocalcinosis and normal kidney function. All the patients were born to consanguineous parents.. Due to limited clinical suspicion and inadequate diagnostic resources in certain countries with limited resources, it is possible for PH to go undiagnosed. The manifestations of the disease can range from no noticeable symptoms to severe disease. Interestingly, in some individuals with primary hyperoxaluria, the disease may not exhibit any symptoms until it is triggered by a high intake of dietary oxalate.

Topics: Adult; Child; Female; Humans; Hyperoxaluria, Primary; Kidney; Kidney Calculi; Male; Oxalates; Renal Insufficiency

Oxalate is a small compound found in certain plant-derived foods and is a major component of calcium oxalate (CaOx) kidney stones. Individuals that consume oxalate enriched meals have an increased risk of forming urinary crystals, which are precursors to CaOx kidney stones. We previously reported that a single dietary oxalate load induces nanocrystalluria and reduces monocyte cellular bioenergetics in healthy adults. The purpose of this study was to extend these investigations to identify specific oxalate-mediated mechanisms in monocytes and macrophages. We performed RNA-Sequencing analysis on monocytes isolated from healthy subjects exposed to a high oxalate (8 mmol) dietary load. RNA-sequencing revealed 1,198 genes were altered and Ingenuity Pathway Analysis demonstrated modifications in several pathways including Interleukin-10 (IL-10) anti-inflammatory cytokine signaling, mitochondrial metabolism and function, oxalic acid downstream signaling, and autophagy. Based on these findings, we hypothesized that oxalate induces mitochondrial and lysosomal dysfunction in monocytes and macrophages via IL-10 and reactive oxygen species (ROS) signaling which can be reversed with exogenous IL-10 or Mitoquinone (MitoQ; a mitochondrial targeted antioxidant). We exposed monocytes and macrophages to oxalate in an in-vitro setting which caused oxidative stress, a decline in IL-10 cytokine levels, mitochondrial and lysosomal dysfunction, and impaired autophagy in both cell types. Administration of exogenous IL-10 and MitoQ attenuated these responses. These findings suggest that oxalate impairs metabolism and immune response via IL-10 signaling and mitochondrial ROS generation in both monocytes and macrophages which can be potentially limited or reversed. Future studies will examine the benefits of these therapies on CaOx crystal formation and growth in vivo.

Topics: Adult; Calcium Oxalate; Cytokines; Humans; Interleukin-10; Kidney Calculi; Macrophages; Monocytes; Oxalates; Reactive Oxygen Species; RNA

Without effective intervention, primary hyperoxaluria type 1 (PH1) causes oxalate-induced kidney damage, leading to end-stage kidney disease and serious complications throughout the body. Although PH1 carries a heavy burden that impacts quality of life, literature on the experiences of those living with PH1 and caring for patients with PH1 is limited. This study aimed to describe the diagnostic journey in PH1 and characterize patients' and caregivers' self-reported experiences throughout the disease course.. This was an observational study involving in-depth, semi-structured telephone interviews. Dominant trends were assessed using constant comparative analysis to identify themes in interviewees' descriptions of their experiences. Individuals aged ≥ 12 years and caregivers of children aged 6-17 years with genetically confirmed PH1 were eligible. Informed consent/assent and ability to read and speak English were required.. Interviewees (16 patients, 12 caregivers) reported a prolonged diagnostic journey due to low disease awareness, among other factors. Upon diagnosis, PH1 was frequently symptomatic, typically involving kidney stone-related symptoms but also potentially symptoms arising beyond the kidneys. PH1 most commonly led to worry and social impairment in adolescents, impaired physical function in adults, and a range of impacts on caregivers. In late-stage disease, dialysis was the most burdensome aspect of living with PH1 (due to time requirements, limitations from living with a catheter, etc.), and this burden was exacerbated by the COVID-19 pandemic. Benefits desired from PH1 management included reductions in laboratory measures of oxalate burden, kidney stone and urination frequency, and oxalate-related skin ulcers.. PH1 greatly impacts patients' and caregivers' lives, primarily due to burdensome disease manifestations and associated emotional, physical, and practical impacts, as well as disease management challenges - particularly those related to dialysis in late-stage disease.

Topics: Adolescent; Adult; Child; Humans; Hyperoxaluria, Primary; Kidney Calculi; Oxalates; Pandemics; Patient Outcome Assessment; Quality of Life; Renal Dialysis

Kidney stones commonly occur with a 50% recurrence rate within 5 years, and can elevate the risk of chronic kidney disease. Macrophage-to-myofibroblast transition (MMT) is a newly discovered mechanism that leads to progressive fibrosis in different forms of kidney disease. In this study, we aimed to investigate the role of MMT in renal fibrosis in glyoxylate-induced kidney stone mice and the mechanism by which signal transducer and activator of transcription 6 (STAT6) regulates MMT.. We collected non-functioning kidneys from patients with stones, established glyoxylate-induced calcium oxalate stone mice model and treated AS1517499 every other day in the treatment group, and constructed a STAT6-knockout RAW264.7 cell line. We first screened the enrichment pathway of the model by transcriptome sequencing; detected renal injury and fibrosis by hematoxylin eosin staining, Von Kossa staining and Sirius red staining; detected MMT levels by multiplexed immunofluorescence and flow cytometry; and verified the binding site of STAT6 at the PPARα promoter by chromatin immunoprecipitation. Fatty acid oxidation (FAO) and fibrosis-related genes were detected by western blot and real-time quantitative polymerase chain reaction.. In this study, we found that FAO was downregulated, macrophages converted to myofibroblasts, and STAT6 expression was elevated in stone patients and glyoxylate-induced kidney stone mice. The promotion of FAO in macrophages attenuated MMT and upregulated fibrosis-related genes induced by calcium oxalate treatment. Further, inhibition of peroxisome proliferator-activated receptor-α (PPARα) eliminated the effect of STAT6 deletion on FAO and fibrosis-associated protein expression. Pharmacological inhibition of STAT6 also prevented the development of renal injury, lipid accumulation, MMT, and renal fibrosis. Mechanistically, STAT6 transcriptionally represses PPARα and FAO through cis-inducible elements located in the promoter region of the gene, thereby promoting MMT and renal fibrosis.. These findings establish a role for STAT6 in kidney stone injury-induced renal fibrosis, and suggest that STAT6 may be a therapeutic target for progressive renal fibrosis in patients with nephrolithiasis.

Topics: Animals; Calcium Oxalate; Fatty Acids; Fibrosis; Glyoxylates; Humans; Kidney; Kidney Calculi; Macrophages; Mice; Myofibroblasts; Oxalates; PPAR alpha; STAT6 Transcription Factor

Inquiry of microbiota involvement in kidney stone disease (KSD) has largely focussed on potential oxalate handling abilities by gut bacteria and the increased association with antibiotic exposure. By systematically comparing the gut, urinary, and oral microbiota of 83 stone formers (SF) and 30 healthy controls (HC), we provide a unified assessment of the bacterial contribution to KSD.. Amplicon and shotgun metagenomic sequencing approaches were consistent in identifying multi-site microbiota disturbances in SF relative to HC. Biomarker taxa, reduced taxonomic and functional diversity, functional replacement of core bioenergetic pathways with virulence-associated gene markers, and community network collapse defined SF, but differences between cohorts did not extend to oxalate metabolism.. We conclude that multi-site microbiota alteration is a hallmark of SF, and KSD treatment should consider microbial functional restoration and the avoidance of aberrant modulators such as poor diet and antibiotics where applicable to prevent stone recurrence. Video Abstract.

Topics: Bacteria; Humans; Kidney Calculi; Metagenome; Microbiota; Oxalates

Nephrolithiasis is a multifactor disease that produces nephrolites in the kidneys. Calcium oxalate hydrate (dihydrated, COD, or monohydrated, COM) stones are the most common ones with more than sixty percent incidence worldwide. They are related to different pathologies, COD with hypercalciuria and COM with hyperoxaluria. COD is an unstable species and transforms into COM (herein named TRA to distinguish the origin of the monohydrated species). TRA and COM are chemically and crystallographically identical leading to misdiagnosis and recurrence increase. In the current study, the composition and crystalline structures of several calcium oxalate stones, classified by morpho-constitutional analysis, were examined by IR and synchrotron through-the-substrate micro-X-ray diffraction (tts-μXRD). Both IR and linear diffractogram studies were able to distinguish between the monohydrated and dihydrated phases but not between COM and TRA, as expected. The analysis of 2D diffraction patterns revealed that TRA showed a lower degree of crystallinity and less texture with respect to COM which can be used as a signature to distinguish between the two. This study confirms that despite the subtle differences between COM and TRA, the origin of the monohydrate oxalates can be unraveled using tts-μXRD. This valuable information should be taken into account in order to improve patients' diagnosis and reduce recurrence by considering and treating the origin of the formed stones.

Topics: Calcium Oxalate; Humans; Kidney Calculi; Oxalates; Synchrotrons; X-Ray Diffraction

One limitation of the use of 24-hour collection is impracticality. We analysed the performance of spot urine measurements to estimate 24-hour excretion in patients with kidney stones.. A total of 74 adult patients from two centres performed a 24-hour urine collection. A sample of the last micturition was sent for spot urine analysis. Twenty patients were asked to collect two additional spot urine samples, one before dinner and the other after dinner. Urinary concentrations of creatinine, calcium, oxalate, uric acid, citrate and magnesium were measured in the 24-hour and each of the spot urine samples. Four approaches were used to estimate 24-hour urinary excretion, multiplying the ratio of the spot urinary analyte to creatinine concentration by (i) measured 24-hour urinary creatinine excretion (Prediction 1), (ii) estimated 24-hour urinary creatinine excretion (Prediction 2), (iii) assumed 1-g 24-hour urinary creatinine excretion (Prediction 3) or (iv) assumed 1.5-g 24-hour urinary creatinine excretion (Prediction 4). For each parameter we computed Lin's concordance correlation coefficients (CCCs), Bland-Altman plots and 95% limits of agreement.. The performance of estimates obtained with Prediction 1 and Prediction 2 was similar, except for citrate and uric acid, for which Prediction 2 performed worse. Both approaches performed moderately well: citrate CCC {0.82 [95% confidence interval (CI) 0.75-0.90]}, oxalate [0.66 (95% CI 0.55-0.78)], magnesium [0.66 (95% CI 0.54-0.77)], calcium [0.63 (95% CI 0.50-0.75)] and uric acid [0.52 (95% CI 0.36-0.68)]. The performance of Predictions 3 and 4 was worse.. Although spot urine samples may hold promise for clinical and population-based research, at present they have limited utility in clinical practice. Measuring or estimating 24-hour creatinine, rather than assuming a given creatinine excretion, will be necessary in future studies of spot urine samples.

Topics: Adult; Calcium; Calcium, Dietary; Citrates; Citric Acid; Creatinine; Humans; Kidney Calculi; Magnesium; Oxalates; Uric Acid

Oxalate exposure to human renal epithelial cells triggers a vicious cycle of oxidative stress leading to cellular injury and deposition of calcium oxalate crystals on the injured cells. This results in further oxidative damage causing inflammation and loss of cell-cell adhesion factors, ultimately leading to irreparable kidney damage. However, these events can be attenuated or prevented by plants rich in antioxidants used in the traditional system of medicine for treatment of kidney stones. To delineate the mechanism by which Bergenia ligulata extract exerts its cytoprotective role in oxalate-induced injury we designed this study. Our results revealed that oxalate-injured HK2 cells cotreated with ethanolic extract of Bergenia ligulata displayed increased viability, reduced oxidative stress due to lowered production of intracellular reactive oxygen species (ROS) and decreased apoptosis. We also observed lowered markers of inflammation, along with increased expression of epithelial marker E-cadherin and decreased expression of mesenchymal markers Vimentin, F-actin, Transforming growth factor beta 1 (TGF-β1) and EMT-related proteins in renal tubular epithelial cells through immunocytochemistry, real-time PCR and western blotting. Our findings collectively suggest that by reducing oxidative stress, modulating crystal structure and preventing crystal-cell adhesion, B. ligulata inhibits the EMT pathway by downregulating the various mediators and thereby exerts its cytoprotective effect.

Topics: Epithelial Cells; Epithelial-Mesenchymal Transition; Female; Humans; Inflammation; Kidney Calculi; Male; Oxalates; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Plant Extracts; Transforming Growth Factor beta1

The role of the gut microbiome in the development of renal stone diseases has not been well characterized. This study focused on the taxonomic and functional profiles of gut microbiomes according to the prevalence and incidence of nephrolithiasis. Stool samples from 915 Korean adults were collected at baseline. Participants were followed for a median of 4.0 years. We evaluated the biodiversity of the gut microbiota and taxonomic profiles associated with nephrolithiasis status, using 16S rRNA gene sequencing. Nephrolithiasis status was categorized into three groups: control (no-stone at both baseline and follow-up visits), incidental nephrolithiasis, and prevalent nephrolithiasis. Compared to the control and incidental nephrolithiasis, the prevalent nephrolithiasis showed a reduced evenness in alpha diversity. Nephrolithiasis was associated with a reduced abundance of some key taxa involved in short-chain fatty acid production. Moreover, the abundance of Bifidobacterium, which possess oxalate-degrading ability, was higher in the control. Conversely, there was no significant difference in the bacterial composition between the incidental and prevalent nephrolithiasis. In our study with repeated nephrolithiasis measurements, prevalent renal stones were associated with an altered gut microbiota composition compared to the control. Besides the known oxalate degradation pathway, other functional pathways inferred in this study require further investigation.

Topics: Adult; Female; Gastrointestinal Microbiome; Humans; Incidence; Kidney Calculi; Male; Oxalates; Prevalence; RNA, Ribosomal, 16S

Topics: Humans; Kidney; Kidney Calculi; Microbiota; Oxalates

The odds of nephrolithiasis increase with more metabolic syndrome (MetS) traits. We evaluated associations of metabolic and dietary factors from urine studies and stone composition with MetS traits in a large cohort of stone-forming patients.. Patients >18 years old who were evaluated for stones with 24-hour urine collections between July 2009 and December 2018 had their records reviewed retrospectively. Patient factors, laboratory values, and diagnoses were identified within 6 months of urine collection and stone composition within 1 year. Four groups with none, one, two, and three or four MetS traits (hypertension, obesity, dyslipidemia, and diabetes) were evaluated. Trends across groups were tested using linear contrasts in analysis of variance and analysis of covariance.. A total of 1473 patients met the inclusion criteria (835 with stone composition). MetS groups were 684 with no traits, 425 with one trait, 211 with two traits, and 153 with three or four traits. There were no differences among groups for urine volume, calcium, or ammonium excretion. There was a significant trend (. Stone-forming patients with MetS have a defined pattern of metabolic and dietary risk factors that contribute to an increased risk of stone formation, including higher acid excretion, largely the result of greater protein intake, and lower urine pH.

Topics: Adolescent; Citrates; Humans; Kidney Calculi; Metabolic Syndrome; Oxalates; Retrospective Studies

Data are scarce regarding dietary risk factors for pediatric nephrolithiasis. Our objective was to perform a case-control study (nonmatched) of the association of dietary nutrients with pediatric urolithiasis.. We obtained dietary information from pediatric urolithiasis patients (from stone clinic in 2013-2016) and healthy controls (well-child visit at primary care in 2011-2012). Survey results were converted to standard nutrient intakes. Children younger than 5 years of age and those with extreme calorie intake values (<500 or >5,000 kcal/day) were excluded. The association of individual nutrients with urolithiasis was assessed by bivariate analysis results and machine-learning methods. A multivariable logistic regression model was fitted using urolithiasis as the outcome.. We included 285 patients (57 stones/228 controls). Mean±SD age was 8.9±3.6 years (range 5-20). Of the patients 47% were male. After adjusting for age, sex, body mass index (obese/overweight/normal), calorie intake and oxalate, urolithiasis was associated with higher dietary sodium (OR=2.43 [95% CI=1.40-4.84] per quintile increase, p=0.004), calcium (OR=1.73 [95% CI=1.07-3.00] per quintile increase, p=0.034) and beta carotene (OR=2.01 [95% CI=1.06-4.18] per quintile increase, p=0.042), and lower potassium (OR=0.31 [95% CI=0.13-0.63] per quintile increase, p=0.003). Sensitivity analysis was performed by removing oxalate from the model and limiting the sample to patients aged 5-13 years, with similar results.. In our cohort, higher dietary intake of calcium, sodium and beta carotene, and lower potassium intake were associated with pediatric urolithiasis. This is the first study using a detailed dietary survey to identify dietary risk factors for pediatric urolithiasis. Further research is warranted to delineate the mechanisms and to generate a lower risk diet profile for pediatric urolithiasis.

Topics: beta Carotene; Calcium; Calcium, Dietary; Case-Control Studies; Child; Child, Preschool; Diet; Female; Humans; Kidney Calculi; Male; Oxalates; Potassium; Risk Factors; Urolithiasis

The dietary patterns are closely associated with gut microbiota, which has been proved associated with kidney stones. To assess the association among the dietary patterns, gut microbiota, and kidney stones, patients with calcium oxalate stones and participants without kidney stones were recruited in West China Hospital and were divided into the low nephrolithiasis risk (LNR) and high nephrolithiasis risk (HNR) dietary pattern group based on the results of food frequency questionnaires. The genomic DNA of the fecal samples were extracted for 16S ribosomal RNA gene sequencing. The non-kidney stone (NS) group comprised 39 LNR and 45 HNR individuals, while the kidney stone (KS) group consisted of 19 LNR and 50 HNR individuals. The distribution of oxalate in urine (p < 0.01) but not calcium (p = 0.741) was significantly varied among the four groups. Significant difference was found in the dietary patterns of people with KS and NS controls (X

Topics: Bacteria; Calcium Oxalate; Calcium, Dietary; Gastrointestinal Microbiome; Humans; Kidney Calculi; Oxalates

Meals rich in oxalate are associated with calcium oxalate (CaOx) kidney stone disease. Hydroxy-L-proline (HLP) is an oxalate precursor found in milk and collagen-containing foods. HLP has been shown to induce CaOx crystal formation in rodents. The purpose of this study was to evaluate the effect of HLP induced oxalate levels on inflammation and renal leukocytes during crystal formation. Male Sprague-Dawley rats (6-8 weeks old) were fed a control diet containing no oxalate for 3 days before being randomized to continue the control diet or 5% HLP for up to 28 days. Blood, 24 h urine, and kidneys were collected on Days 0, 7, 14, or 28. Urinary oxalate levels, crystal deposition, and renal macrophage markers were evaluated using ion chromatography-mass spectrometry, immunohistochemistry, and qRT-PCR. Renal leukocytes were assessed using flow cytometry and RNA-sequencing. HLP feeding increased urinary oxalate levels and renal crystal formation in animals within 7 days. HLP also increased renal macrophage populations on Days 14 and 28. Transcriptome analysis revealed that renal macrophages from animals fed HLP for 7 days were involved in inflammatory response and disease, stress response to LPS, oxidative stress, and immune cell trafficking. Renal macrophages isolated on Day 14 were involved in cell-mediated immunological pathways, ion homeostasis, and inflammatory response. Collectively, these findings suggest that HLP-mediated oxalate levels induce markers of inflammation, leukocyte populations, and reprograms signaling pathways in macrophages in a time-dependent manner. Additional studies investigating the significance of oxalate on renal macrophages could aid in our understanding of kidney stone formation.

Topics: Animals; Calcium Oxalate; Hydroxyproline; Inflammation; Kidney Calculi; Macrophages; Male; Nephrolithiasis; Oxalates; Rats; Rats, Sprague-Dawley

Nephrolithiasis is a common and recurrent disease affecting 9% of the US population. Hyperoxaluria is major risk factor for calcium oxalate kidney stones, which constitute two-thirds of all kidney stones. SLC26A3 (DRA, downregulated in adenoma) is an anion exchanger of chloride, bicarbonate, and oxalate thought to facilitate intestinal oxalate absorption, as evidenced by approximately 70% reduced urine oxalate excretion in knockout mice. We previously identified a small-molecule SLC26A3 inhibitor (DRAinh-A270) that selectively inhibited SLC26A3-mediated chloride/bicarbonate exchange (IC50 ~ 35 nM) and, as found here, oxalate/chloride exchange (IC50 ~ 60 nM). In colonic closed loops in mice, luminal DRAinh-A270 inhibited oxalate absorption by 70%. Following oral sodium oxalate loading in mice, DRAinh-A270 largely prevented the 2.5-fold increase in urine oxalate/creatinine ratio. In a mouse model of oxalate nephropathy produced by a high-oxalate low-calcium diet, vehicle-treated mice developed marked hyperoxaluria with elevated serum creatinine, renal calcium oxalate crystal deposition, and renal injury, which were largely prevented by DRAinh-A270 (10 mg/kg twice daily). DRAinh-A270 administered over 7 days to healthy mice did not show significant toxicity. Our findings support a major role of SLC26A3 in intestinal oxalate absorption and suggest the therapeutic utility of SLC26A3 inhibition for treatment of hyperoxaluria and prevention of calcium oxalate nephrolithiasis.

Topics: Animals; Antiporters; Bicarbonates; Calcium Oxalate; Chlorides; Hyperoxaluria; Kidney Calculi; Mice; Oxalates; Sulfate Transporters

The ossification of renal tubular epithelial cells (RTECs) plays an important initial role in the formation of kidney stones, but its specific mechanism is still unclear. The JAK2/STAT3 signaling pathway is important for bone cell differentiation. Accordingly, we explored the role and mechanism of the JAK2/STAT3 signaling pathway in the ossification of RTECs.. We used oxalate or ethylene glycol to construct kidney stone models in vitro and in vivo, and investigated the expression of osteogenic-specific genes, osteogenesis ability, and JAK2/STAT3 signaling in the kidney stone models by western blotting, qRT-PCR, immunofluorescence, and immunohistochemistry. Then, genetic engineering or drugs were used to inhibit the expression or activation of JAK2, and the expression of osteogenic-specific genes and the osteogenic ability of the RTECs were determined again.. In the in vitro and in vivo kidney stone models, the expression of osteogenic specific genes in the RTECs was significantly upregulated, the osteogenic capacity was significantly increased, and the expression of p-JAK2 (phospho-JAK2) and p-STAT3 (phospho-STAT3) was significantly increased. When the expression or activation of JAK2 was inhibited, the ossification of RTECs and the formation of kidney stones was reversed.. During the formation of kidney stones, RTECs undergo obvious ossification, and the JAK2/STAT3 signaling pathway plays a key positive regulatory role in this process.

Topics: Cell Differentiation; Humans; Janus Kinase 2; Kidney Calculi; Osteogenesis; Oxalates; Signal Transduction; STAT3 Transcription Factor

Medically complex, non-ambulatory children can often suffer from nephrolithiasis. The purpose of this study is to determine risk factors which are predictive for recurrent stone formation in this patient population.. A retrospective cohort study was performed on non-ambulatory patients with cerebral palsy and/or severe developmental delay presenting to a high-volume Pediatric Stone Center from 2015 to 2019. Two 24-hour urine collections were performed as a baseline prior to pharmacotherapeutic and/or dietary intervention. Healthy stone-forming children served as a control group.. Urinary oxalate excretion is significantly increased in a cohort of medically complex, non-ambulatory stone-forming children. Urinary calcium excretion was not elevated between study subjects and healthy controls. Further analysis is needed to assess if dietary intervention to limit oxalate excretion results in decreased stone formation.

Topics: Calcium; Calcium Oxalate; Child; Enteral Nutrition; Humans; Kidney Calculi; Nephrolithiasis; Oxalates; Retrospective Studies

To help guide empiric therapy for kidney stone disease, we sought to demonstrate the feasibility of predicting 24-hour urine abnormalities using machine learning methods.. We trained a machine learning model (XGBoost [XG]) to predict 24-hour urine abnormalities from electronic health record-derived data (n = 1314). The machine learning model was compared to a logistic regression model [LR]. Additionally, an ensemble (EN) model combining both XG and LR models was evaluated as well. Models predicted binary 24-hour urine values for volume, sodium, oxalate, calcium, uric acid, and citrate; as well as a multiclass prediction of pH. We evaluated performance using area under the receiver operating curve (AUC-ROC) and identified predictors for each model.. The XG model was able to discriminate 24-hour urine abnormalities with fair performance, comparable to LR. The XG model most accurately predicted abnormalities of urine volume (accuracy = 98%, AUC-ROC = 0.59), uric acid (69%, 0.73) and elevated urine sodium (71%, 0.79). The LR model outperformed the XG model alone in prediction of abnormalities of urinary pH (AUC-ROC of 0.66 vs 0.57) and citrate (0.69 vs 0.64). The EN model most accurately predicted abnormalities of oxalate (accuracy = 65%, ROC-AUC = 0.70) and citrate (65%, 0.69) with overall similar predictive performance to either XG or LR alone. Body mass index, age, and gender were the three most important features for training the models for all outcomes.. Urine chemistry prediction for kidney stone disease appears to be feasible with machine learning methods. Further optimization of the performance could facilitate dietary or pharmacologic prevention.

Topics: Citrates; Citric Acid; Humans; Kidney Calculi; Machine Learning; Oxalates; Sodium; Uric Acid

American Urology Association guidelines recommend genetic testing for patients with recurrent stones and urine oxalate > 75 mg/day. The goal of this study was to examine the treatment of patients in this category in a large multidisciplinary adult stone clinic.. Patients were evaluated from a single institution between 2006 and 2019. Those with at least one level of urinary oxalate excretion (uOx) above 75 mg/day were identified. A chart review identified enteric risk factors and genetic testing results. Patients without an identifiable enteric cause were considered idiopathic.. A total of 4229 separate 24-h urine collections in 1302 patients were reviewed. At least one measurement of uOx above 75 mg/day was found in 103 (7.9%) patients. Enteric hyperoxaluria (EH) was seen in 28 (27%) and idiopathic hyperoxaluria (IH) in 76 (74%). 20 (71%) patients in the EH group had undergone gastric bypass. The median uOx was significantly higher level in the EH group (121.0 vs. 93.0 mg/day). For the entire cohort, there was a drop in uOx (- 33.8 mg/day) with medical and dietary therapy after a follow-up of 46.6 months. The final oxalate was higher in EH (88.9 vs. 60.1 mg/day). Only one patient had referral for genetic testing and was found to have primary hyperoxaluria type 2.. The most common cause of significant hyperoxaluria in patients with recurrent nephrolithiasis remains idiopathic. Patients with IH have more significant improvement in uOx compared to EH; however, both groups had hyperoxaluria at last follow-up. Rate of genetic testing is low despite guideline recommendations.

Topics: Adult; Cohort Studies; Humans; Hyperoxaluria; Kidney Calculi; Nephrolithiasis; Oxalates; Risk Factors

Kidney stones are composed of approximately 70-80% calcium oxalate. However, the exact mechanism of formation of calcium oxalate kidney stones remains unclear. In this study, we investigated the roles of endoplasmic reticulum stress (ERS), reactive oxygen species (ROS), and the NF-κB signalling pathway in the pathogenesis of oxalate-induced renal tubular epithelial cell injury and its possible molecular mechanisms.. We established a model to evaluate the formation of kidney stones by intraperitoneal injection of glyoxylic acid solution into mice and assessed cell morphology, apoptosis, and the expression levels of ERS, ROS, and NF-κB signalling pathway-related proteins in mouse renal tissues. Next, we treated HK-2 cells with potassium oxalate to construct a renal tubular epithelial cell injury model. We detected the changes in autophagy, apoptosis, and mitochondrial membrane potential and investigated the ultrastructure of the cells by transmission electron microscopy. Western blotting revealed the expression levels of apoptosis and autophagy proteins; mitochondrial structural and functional proteins; and ERS, ROS, and NF-κB (p65) proteins. Lastly, we studied the downregulation of NF-κB activity in HK-2 cells by lentivirus interference and confirmed the interaction between the NF-κB signalling and ERS/ROS pathways.. We observed swelling of renal tissues, increased apoptosis of renal tubular epithelial cells, and activation of the ERS, ROS, and NF-κB signalling pathways in the oxalate group. We found that oxalate induced autophagy, apoptosis, and mitochondrial damage in HK-2 cells and activated the ERS/ROS/NF-κB pathways. Interestingly, when the NF-κB signalling pathway was inhibited, the ERS/ROS pathway was also inhibited.. Oxalate induces HK-2 cell injury through the interaction between the NF-κB signalling and ERS/ROS pathways.

Topics: Animals; Apoptosis; Calcium Oxalate; Endoplasmic Reticulum Stress; Epithelial Cells; Kidney Calculi; Mice; NF-kappa B; Oxalates; Reactive Oxygen Species

Oxalate and citrate in 24 h urine and serum are considered to be associated with the incidence and recurrence risk of calcium oxalate kidney stones. The quantification of oxalate and citrate contributes to understand the pathological metabolism of kidney stones and guide the early diagnosis and recurrence monitoring. Although simultaneous quantification of oxalate and citrate in urine using liquid chromatography tandem mass spectrometry (LC-MS/MS) have been reported, the optimization of chromatographic column, mobile phase and mass spectrometry (MS) parameters has not been performed. In addition, these is a lack of suitable method for simultaneous detection of oxalate and citrate both in serum and urine. Therefore, we developed a method for the simultaneous determination of oxalate and citrate in urine and serum based on ion-pairing reversed-phase (IP-RP) LC-MS/MS. Herein, five ion-pair reagents, namely, triethanolamine, dimethylbutyl amine, diisopropenyl amine, N,N-dimethylcyclohexylamine and tripropylamine, and three ion-pairing reagent (IPR) buffers, namely, acetic acid, hexafluoro-2-isopropanol, and hexafluoro-2-methyl-2-propanol, were compared in regard to their chromatographic peak abundance and separation of oxalate and citrate. Moreover, MS parameters and the multiple reaction monitoring (MRM) conditions were also evaluated and optimized to obtain the maximum peak abundance. After that, the method was validated in the linear range of 0.25-1000 µM, and the correlation coefficient was ≥ 0.99. The precision and accuracy were < 14.70% and < 19.73%, respectively. The extraction recovery was 80.53-108.79%, and the matrix effect was < 8.79%. The quality control samples were stable at room temperature for 4 h, 4 °C for 24 h, and for 3 freeze-thaw cycles. Finally, this method was applied to the determination of oxalate and citrate in the serum and urine of rats with calcium oxalate kidney stones. The establishment of a stable and effective oxalate and citrate detection method is conducive to the diagnosis and monitoring of kidney stones.

Topics: Amines; Animals; Calcium Oxalate; Chromatography, Liquid; Citric Acid; Ions; Kidney Calculi; Nephrolithiasis; Oxalates; Rats; Tandem Mass Spectrometry

We examined how physicians made therapeutic choices to decrease stone risk in patients with bowel disease without colon resection, many of whom have enteric hyperoxaluria (EH), at a single clinic. We analyzed clinic records and 24-h urine collections before and after the first clinic visit, among 100 stone formers with bowel disease. We used multivariate linear regression and t tests to compare effects of fluid intake, alkali supplementation, and oxalate-focused interventions on urine characteristics. Patients advised to increase fluid intake had lower initial urine volumes (L/day; 1.3 ± 0.5 vs. 1.7 ± 0.7) and increased volume more than those not so advised (0.7 ± 0.6 vs. 0.3 ± 0.6 p = 0.03; intervention vs. non-intervention). Calcium oxalate supersaturation (CaOx SS) fell (95% CI -4.3 to -0.8). Alkali supplementation increased urine pH (0.34 ± 0.53 vs. 0.22 ± 0.55, p = 0.26) and urine citrate (mg/d; 83 ± 256 vs. 98 ± 166, p = 0.74). Patients advised to reduce oxalate (mg/day) absorption had higher urine oxalate at baseline (88 ± 44 vs. 50 ± 26) which was unchanged on follow-up (88 (baseline) vs. 91 (follow-up), p = 0.90). Neither alkali (95% CI -1.4 to 2.1) nor oxalate-focused advice (95% CI -1.2 to 2.3) lowered CaOx SS. Physicians chose treatments based on baseline urine characteristics. Advice to increase fluid intake increased urine volume and decreased CaOx SS. Alkali and oxalate interventions were ineffective.

Topics: Alkalies; Calcium Oxalate; Humans; Hyperoxaluria; Kidney Calculi; Oxalates

DSP0 was carboxymethylated with chloroacetic acid at varying degrees. Then, oxalate-damaged HK-2 cells were repaired with modified polysaccharide, and the changes in biochemical indices before and after repair were detected.. Three modified polysaccharides with 7.45% (CDSP1), 12.2% (CDSP2), and 17.7% (CDSP3) -COOH are obtained. Compared with DSP0 (-COOH content = 1.17%), CDSPs have stronger antioxidant activity in vitro and can improve the vitality of damaged HK-2 cells. CDSPs repair the cell morphology and cytoskeleton, increase the cell healing ability, reduce reactive oxygen species and nitric oxide levels, increase mitochondrial membrane potential, limit autophagy level to a low level, reduce the eversion of phosphatidylserine in the cell membrane, weaken the inhibition of oxalate on DNA synthesis, restore cell cycle to normal state, promote cell proliferation, and reduce apoptosis/necrosis.. The carboxymethylation modification of DSP0 can improve its antioxidant activity and enhance its ability to repair damaged HK-2 cells. Among them, CDSP2 with medium -COOH content has the highest activity of repairing cells, whereas CDSP3 with the highest -COOH content has the highest antioxidant activity. This difference may be related to the active environment of polysaccharide and conformation of the polysaccharide and cell signal pathway. This result suggests that

Topics: Antioxidants; Humans; Kidney Calculi; Oxalates; Polysaccharides; Reactive Oxygen Species

Nephrolithiasis is one of the most common and frequent urologic diseases worldwide. The molecular mechanism of kidney stone formation is complex and remains to be illustrated. Transcript factors (TFs) that influenced the expression pattern of multiple genes, as well as microRNAs, important posttranscriptional modulators, play vital roles in this disease progression. Datasets of nephrolithiasis mice and kidney stone patients were acquired from Gene Expression Omnibus repository. TFs were predicted from differentially expressed genes by RcisTarget. The target genes of differential-expressed microRNAs were predicted by miRWalk. MicroRNA-mRNA network and PPI network were constructed. Functional enrichment analysis was performed via Metascape and Cytoscape identified hub genes. The assay of quantitative real-time PCR (q-PCR) and immunochemistry and the datasets of oxalate diet-induced nephrolithiasis mice kidneys and kidney stone patients' samples were utilized to validate the bioinformatic results. We identified three potential key TFs (Egr1, Rxra, Max), which can be modulated by miR-181a-5p, miR-7b-3p and miR-22-3p, respectively. The TFs and their regulated hub genes influenced the progression of nephrolithiasis via altering the expression of genes enriched in the functions of fibrosis, cell proliferation and molecular transportation and metabolism. The expression changes of transcription factors were consistent in q-PCR and immunochemistry results. For regulated hub genes, they showed consistent expression changes in oxalate diet-induced nephrolithiasis mice model and human kidneys with stones. The identified and verified three TFs, which may be modulated by microRNAs in nephrolithiasis disease progression, mainly influence biological processes responding to fibrosis, proliferation and molecular transportation and metabolism. The transcript influence showed consistency in multiple nephrolithiasis mice models and kidney stone patients.

Topics: Animals; Disease Progression; Early Growth Response Protein 1; Fibrosis; Gene Expression Profiling; Gene Regulatory Networks; Humans; Kidney Calculi; Mice; MicroRNAs; Oxalates; Retinoid X Receptor alpha; RNA, Messenger

Sex-specific differences in nephrolithiasis with respect to both distribution of prevalence and stone composition are widely described and may be influenced by sex hormones.. We conducted a cross-sectional analysis of the relationship between 24-h urinary sex hormone metabolites measured by gas chromatography-mass spectrometry with urinary calcium, oxalate and citrate excretion in a cohort of 628 kidney stone formers from a tertiary care hospital in Switzerland, taking demographic characteristics, kidney function and dietary factors into account.. We observed a positive association of urinary calcium with urinary testosterone and 17β-oestradiol. Positive associations of urinary calcium with dehydroepiandrosterone (DHEA), 5α-DH-testosterone, aetiocholanolone, androsterone and oestriol were modified by net gastrointestinal alkali absorption or urinary sulphate excretion. As the only sex hormone, DHEA was inversely associated with urinary oxalate excretion in adjusted analyses. Urinary citrate correlated positively with urinary testosterone. Associations of urinary citrate with urinary androsterone, 17β-oestradiol and oestriol were modified by urinary sulphate or sodium or by sex.. Urinary androgens and oestrogens are significantly associated with urinary calcium and citrate excretion and associations are modified in part by diet. Our data furthermore reveal DHEA as a novel factor associated with urinary oxalate excretion in humans.

Topics: Calcium; Citrates; Citric Acid; Cross-Sectional Studies; Female; Gonadal Steroid Hormones; Humans; Kidney Calculi; Male; Oxalates

Patients with kidney stones are counseled to eat a diet low in animal protein, sodium, and oxalate and rich in fruits and vegetables, with a modest amount of calcium, usually from dairy products. Restriction of sodium, potassium, and oxalate may also be recommended in patients with chronic kidney disease. Recently, plant-based diets have gained popularity owing to health, environmental, and animal welfare considerations. Our objective was to compare concentrations of ingredients important for kidney stones and chronic kidney disease in popular brands of milk alternatives.. Sodium, calcium, and potassium contents were obtained from nutrition labels. The oxalate content was measured by ion chromatography coupled with mass spectrometry.. The calcium content is highest in macadamia followed by soy, almond, rice, and dairy milk; it is lowest in cashew, hazelnut, and coconut milk. Almond milk has the highest oxalate concentration, followed by cashew, hazelnut, and soy. Coconut and flax milk have undetectable oxalate levels; coconut milk also has comparatively low sodium, calcium, and potassium, while flax milk has the most sodium. Overall, oat milk has the most similar parameters to dairy milk (moderate calcium, potassium and sodium with low oxalate). Rice, macadamia, and soy milk also have similar parameters to dairy milk.. As consumption of plant-based dairy substitutes increases, it is important for healthcare providers and patients with renal conditions to be aware of their nutritional composition. Oat, macadamia, rice, and soy milk compare favorably in terms of kidney stone risk factors with dairy milk, whereas almond and cashew milk have more potential stone risk factors. Coconut milk may be a favorable dairy substitute for patients with chronic kidney disease based on low potassium, sodium, and oxalate. Further study is warranted to determine the effect of plant-based milk alternatives on urine chemistry.

Topics: Animals; Calcium; Calcium, Dietary; Diet, Sodium-Restricted; Female; Humans; Kidney Calculi; Male; Oxalates; Potassium; Renal Insufficiency, Chronic; Risk Factors; Sodium

Renal tubular epithelial cell damage is the basis for the formation of kidney stones. Oxalate can induce human proximal tubular (HK-2) cells to undergo autophagy and ferroptosis. The present study was aimed at investigating whether the ferroptosis of HK-2 cells induced by oxalate is caused by the excessive activation of autophagy. We treated HK-2 cells with 2 mmol/L of oxalate to establish a kidney stone model. First, we tested the degree of oxidative damage and the level of autophagy and ferroptosis in the control group and the oxalate intervention group. We then knocked down and overexpressed the

Topics: Animals; Autophagy; Epithelial Cells; Ferroptosis; Humans; Kidney Calculi; Male; Oxalates; Rats; Rats, Sprague-Dawley; Transfection

Findings regarding the association between tea and coffee consumption and oxalate-calcium stone are sparse and uncertain. The purpose of this study was to investigate the relations of tea and coffee with the risk of calcium oxalate stone formation. A total sample of 215 newly diagnosed patients with calcium oxalate stones and 215 controls matched for sex and age were recruited. Dietary intake of participants was assessed using a validated food frequency questionnaire over the preceding year and participants were asked to determine how many glasses of tea and cups of coffee they usually use. The associations between tea and coffee and kidney stone were examined using multivariable logistic regression. Compared with controls, cases had greater intake of tea (2.18±0.76 vs. 1.82±0.79 glasses/d) but lower intake of coffee (1.18±0.38 vs. 1.26±0.44 cups/week). After adjustment for potential confounders, compared with those who drank <2 glasses of tea/d, individuals with tea consumption of ≥4 glasses/d had greater risk for having calcium oxalate stone (OR= 2.73; 95 % CI: 1.50, 4.99). In the crude model, compared with coffee consumption for <1 cup/week, consumption of ≥1 cup/week was associated with a 38 % decrease in the risk of calcium oxalate stone. However, adjustment for potential confounders disappeared the significance (OR=0.81; 95 % CI: 0.48, 1.35). These results suggest that while high consumption of tea is associated with increased risk of calcium oxalate kidney stone, coffee drinking is not pertinent. However, due to low consumption of coffee in this population, our results should be interpreted cautiously.

Topics: Calcium; Coffee; Humans; Kidney Calculi; Oxalates; Risk Factors; Tea

Copious fluid intake is the most essential nutritional measure in the treatment of urolithiasis, and is suggested to be a protective factor in the primary prevention of urinary stone formation. Although the intake of black tea contributes to daily fluid intake, the high oxalate content could outweigh the beneficial effect of urine dilution. The present study investigated the effect of black tea consumption on urinary risk factors for kidney stone formation. Ten healthy men received a standardized diet for a period of ten days. Subjects consumed 1.5 L/day of fruit tea (0 mg/day oxalate) during the 5-day control phase, which was replaced by 1.5 L/day of black tea (86 mg/day oxalate) during the 5-day test phase. Fractional and 24-h urines were obtained. The intake of black tea did not significantly alter 24-h urinary oxalate excretion. Urinary citrate, an important inhibitor of calcium stone formation, increased significantly, while the relative supersaturation of calcium oxalate, uric acid, and struvite remained unchanged. No significantly increased risk for kidney stone formation could be derived from the ingestion of black tea in normal subjects. Further research is needed to evaluate the impact of black tea consumption in kidney stone patients with intestinal hyperabsorption of oxalate.

Topics: Adult; Citric Acid; Drinking; Eating; Humans; Kidney Calculi; Male; Oxalates; Risk Factors; Tea; Time Factors; Uric Acid; Young Adult

This is the first prospective study to investigate the association between kidney stones, bone mineral density, serum testosterone, colon cancer and O. formigenes colonization. 40 kidney stone patients and 85 controls were enrolled. O. formigenes colonization was established. BMD was examined from T- and Z-scores using dual energy absorptiometry. O. formigenes was found in 28 of 40 cases and 80 of 85 controls. BMD was significantly reduced in patients (p < 0.05). The evaluation revealed a significant association between lowered O. formigenes colonization and low testosterone. Urinary calcium and oxalates levels were greater in patient. Serum testosterone and urinary citrate concentrations was reduced in patients with a significant difference. Also an association between O. formigenes and colon cancer was noted. Absence of O. formigenes might stand for a pathogenic factor in calcium oxalate stone, low bone mineral density, low testosterone levels and also colon cancer, when antibiotics are prescribed generously.

Topics: Administration, Oral; Adult; Anti-Bacterial Agents; Bone Density; Calcium; Case-Control Studies; Colonic Neoplasms; Feces; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalobacter formigenes; Prospective Studies; Risk Assessment; Testosterone; Young Adult

Data directly demonstrating the relationship between urinary oxalate (UOx) excretion and stone events in those with enteric hyperoxaluria (EH) are limited. Therefore, we assessed the relationship between UOx excretion and risk of kidney stone events in a retrospective population-based EH cohort. In all, 297 patients from Olmsted County, Minnesota were identified with EH based upon having a 24-h UOx ≥40 mg/24 h preceded by a diagnosis or procedure associated with malabsorption. Diagnostic codes and urologic procedures consistent with kidney stones during follow-up after baseline UOx were considered a new stone event. Logistic regression and accelerated failure time modeling were performed as a function of UOx excretion to predict the probability of new stone event and the annual rate of stone events, respectively, with adjustment for urine calcium and citrate. Mean ± standard deviation age was 51.4 ± 11.4 years and 68% were female. Median (interquartile range) UOx was 55.4 (46.6-73.0) mg/24 h and 81 patients had one or more stone event during a median follow-up time of 4.9 (2.8-7.8) years. Higher UOx was associated with a higher probability of developing a stone event (P < 0.01) and predicted an increased annual risk of kidney stones (P = 0.001). Estimates derived from these analyses suggest that a 20% decrease in UOx is associated with 25% reduction in the annual odds of a future stone event. Thus, these data demonstrate an association between baseline UOx and stone events in EH patients and highlight the potential benefit of strategies to reduce UOx in this patient group.. Data directly demonstrating the relationship between urinary oxalate (UOx) excretion and stone events in those with enteric hyperoxaluria (EH) are limited.. We assessed the relationship between UOx excretion and risk of kidney stone events in a retrospective population-based EH cohort. In all, 297 patients from Olmsted County, Minnesota were identified with EH based upon having a 24-h UOx ≥40 mg/24 h preceded by a diagnosis or procedure associated with malabsorption. Diagnostic codes and urologic procedures consistent with kidney stones during follow-up after baseline UOx were considered a new stone event. Logistic regression and accelerated failure time modeling were performed as a function of UOx excretion to predict the probability of new stone event and the annual rate of stone events, respectively, with adjustment for urine calcium and citrate.. Mean ± SD age was 51.4 ± 11.4 years and 68% were female. Median (interquartile range) UOx was 55.4 (46.6-73.0) mg/24 h and 81 patients had ≥1 stone event during a median follow-up time of 4.9 (2.8-7.8) years. Higher UOx was associated with a higher probability of developing a stone event (P < 0.01) and predicted an increased annual risk of kidney stones (P = 0.001). Estimates derived from these analyses suggest that a 20% decrease in UOx is associated with 25% reduction in the annual odds of a future stone event.. These data demonstrate an association between baseline UOx and stone events in EH patients and highlight the potential benefit of strategies to reduce UOx in this patient group.

Topics: Adult; Female; Humans; Hyperoxaluria; Kidney Calculi; Middle Aged; Oxalates; Retrospective Studies; Urinary Calculi

Our aim was to investigate the validity of osmolality from 24-h urine collection in examining the risk for calcium-oxalate (CaOx) kidney stone formation in patients with recurrent urolithiasis. Three hundred and twelve subjects (males/females: 184/128) from France with a history of recurrent kidney stones from confirmed or putative CaOx origin were retrospectively included in the study (46 ± 14 years, BMI: 25.3 ± 5.0 kg·m

Topics: Calcium; Calcium Oxalate; Crystallization; Female; Humans; Kidney Calculi; Male; Osmolar Concentration; Oxalates; Retrospective Studies; Urinary Calculi; Urolithiasis

Oxalobacter formigenes, as a gram-negative anaerobic bacterium, metabolizes oxalate in the intestine by the enzymes oxalyl-CoA decarboxylase (OXC) and formyl-CoA transferase (FRC). Therefore, not only the presence of the bacterium but also microbial load may affect intestinal absorption and urinary exertion. We evaluated the relationship between Oxalobacter formigenes load and the formation of calcium oxalate urolithiasis using quantitative molecular methods.. By clinical manifestation and stone analysis, we selected the urine and stool specimens of 73 patients with calcium oxalate urolithiasis. First, the gene regions of the two genes FRC and OXC in Oxalobacter formigenes were selected utilizing bioinformatics and specific primers designed for these regions. Following DNA extraction from stool specimens by specific primers of each gene, PCR was carried out and positive samples were sequenced. Then, qPCR was applied to determine the effective load of Oxalobacter. Also, biochemical tests were performed to measure the excretion rate of oxalate in urine specimens.. In addition to oxalobacter identification by PCR, the load of bacteria was quantitatively assessed using qPCR by specific primers for both FRC and OXC gene regions. A significant negative relationship had found between the formation of calcium oxalate urolithiasis and the presence of Oxalobacter formigenes in patients with kidney stone disease. The mean excretion of oxalate and citrate in urolithiasis cases were 22.93 and 552.106 mg/24h, respectively.. The presence of Oxalobacter formigenes can highly inhibit the generation of calcium oxalate urolithiasis. Furthermore, molecular techniques are more effective than other methods such as culture for the isolation of this bacterium.

Topics: Base Composition; Humans; Kidney Calculi; Oxalates; Oxalobacter formigenes; Phylogeny; Real-Time Polymerase Chain Reaction; RNA, Ribosomal, 16S; Sequence Analysis, DNA; Urolithiasis

Previous studies have demonstrated that excretion of urinary extracellular vesicles (EVs) from different nephron segments differs between kidney stone formers and non-stone formers (NSFs), and could reflect pathogenic mechanisms of urinary stone disease. In this study we quantified selected populations of specific urinary EVs carrying protein markers of immune cells and calcium/phosphorus physiology in calcium oxalate stone formers (CSFs) compared to non-stone formers (NSFs).. Biobanked urine samples from CSFs (n = 24) undergoing stone removal surgery and age- and sex- matched NSFs (n = 21) were studied. Urinary EVs carrying proteins related to renal calcium/phosphorus physiology (phosphorus transporters (PiT1 and PiT2), Klotho, and fibroblast growth factor 23 (FGF23); markers associated with EV generation (anoctamin-4 (ANO4) and Huntington interacting protein 1 (HIP1)), and markers shed from activated immune cells were quantified by standardized and published method of digital flow cytometry.. Urine excretion of calcium, oxalate, phosphorus, and calcium oxalate supersaturation (SS) were significantly higher in CSFs compared to NSFs (P < 0.05). Urinary excretion of EVs with markers of total leukocytes (CD45), neutrophils (CD15), macrophages (CD68), Klotho, FGF23, PiT1, PiT2, and ANO4 were each markedly lower in CSFs than NSFs (P < 0.05) whereas excretion of those with markers of monocytes (CD14), T-Lymphocytes (CD3), B-Lymphocytes (CD19), plasma cells (CD138 plus CD319 positive) were not different between the groups. Urinary excretion of EVs expressing PiT1 and PiT2 negatively (P < 0.05) correlated with urinary phosphorus excretion, whereas excretion of EVs expressing FGF23 negatively (P < 0.05) correlated with both urinary calcium and phosphorus excretion. Urinary EVs with markers of HIP1 and ANO4 correlated negatively (P < 0.05) with clinical stone events and basement membrane calcifications on papillary tip biopsies.. Urinary excretion of EVs derived from specific types of activated immune cells and EVs with proteins related to calcium/phosphorus regulation differed between CSFs and NSFs. Further validation of these and other populations of urinary EVs in larger cohort could identify biomarkers that elucidate novel pathogenic mechanisms of calcium stone formation in specific subsets of patients.

Topics: Aged; Antigens, CD; Biomarkers; Calcium Oxalate; Case-Control Studies; Citric Acid; Extracellular Vesicles; Female; Flow Cytometry; Humans; Kidney Calculi; Leukocytes; Macrophages; Male; Middle Aged; Oxalates; Urine

Animal models have demonstrated an interactive relationship between the epithelial anion exchanger SLC26A6 and transporter NaDC-1 that regulates citrate and oxalate homeostasis. This relationship is a potential mechanism to protect against kidney stones as higher urine oxalate is accompanied by higher urine citrate but it has not been explored in humans.. We examined 24-h urine data on 13,155 kidney stone forming patients (SF) from separate datasets at the University of Chicago and Litholink, a national laboratory, and 143 non-kidney stone forming participants (NSF) to examine this relationship in humans. We used multivariate linear regression models to examine the association between oxalate and citrate in all study participants and separately in SF and NSF.. Higher urinary oxalate was associated with higher urinary citrate in both SF and NSF. In NSF, the multivariate adjusted urine citrate excretion was 3.0 (1.5-4.6) (mmol)/creatinine (mmol) per oxalate (mmol)/creatinine (mmol). In SF, the multivariate adjusted urine citrate excretion was 0.3 (0.2-0.4) (mmol)/creatinine (mmol) per oxalate (mmol)/creatinine (mmol).. Higher urinary oxalate excretion was associated with higher urinary citrate excretion and this effect was larger in non-kidney stone forming participants compared with those who form kidney stones.

Topics: Case-Control Studies; Citric Acid; Creatinine; Female; Humans; Kidney Calculi; Linear Models; Male; Middle Aged; Oxalates

Topics: Citrates; Citric Acid; Humans; Kidney Calculi; Oxalates

Topics: Calcium Oxalate; Humans; Kidney Calculi; Nephrolithiasis; Oxalates; Renal Insufficiency, Chronic; Retrospective Studies

Kidney stones are a common threat to the health of elderly patients with a high incidence of disease. However, the specific molecular mechanism of the formation of kidney stones has not been elucidated. Here, we combined signalling molecules with signalling pathways in a double positive circulation regulation model. In addition, we found that LCN2 plays a role in promoting kidney stones through regulation of the ERK signalling pathway and expression of other kidney stone-related genes. LCN2 expression was upregulated upon oxalate stimulation. P-ERK1/2 inhibition by U0126 in kidney epithelial cells resulted in decreased expression of LCN2. Furthermore, the upregulation of LCN2 not only depended on the activation of the ERK signalling pathway but also regulated the activation of the ERK signalling pathway. Importantly, upregulation of LCN2 not only caused kidney epithelial cell damage but also promoted the expression of other kidney stone-related genes. Our findings improved the understanding of LCN2 and might lead to the development of new therapeutic and prognostic markers for kidney stones.

Topics: Epithelial Cells; Feedback, Physiological; HEK293 Cells; Humans; Kidney Calculi; Lipocalin-2; MAP Kinase Signaling System; Oxalates

To investigate potential oxalate-degrading bacteria, including Oxalobacter formigenes, Lactobacillus (Lac) and Bifidobacterium (Bif) genera, and Oxalyl-CoA decarboxylase (oxc) encoding Lac (LX) and Bif (BX) species in participants with recurrent calcium kidney stones, and their correlation with 24-h urine oxalate.. Stool and 24-h urine samples were collected from 58 patients with urolithiasis (29 cases with and 29 without hyperoxaluria) and 29 healthy controls. Absolute quantitation and relative abundance of the bacteria were measured by real-time PCR. The relationship between the investigated bacteria and 24-h urine oxalate were assessed statistically.. The count per gram of stool and relative abundance of O. formigenes, Lac, Bif, LX and BX and the number of participants carrying O. formigenes, LX and BX bacteria were not significantly different between the groups; however, the relative abundance of O. formigenes in the kidney stone group was lower than in healthy controls (P = 0.035). More healthy controls were O. formigenes-positive compared with participants in the kidney stone group (P = 0.052). The results of the linear regression model, including all study participants, showed that the presence of O. formigenes could decrease 24-h urine oxalate (β = -8.4, P = 0.047). Neither Lac and Bif genera nor LX and BX species were correlated with calcium stones or urine oxalate.. These results emphasize the role of O. formigenes in kidney stone formation and its role in hyperoxaluria, which may be independent of kidney stone disease. Moreover, our results suggest that, although some Lac and Bif strains have oxalate-degrading potential, they may not be among the major oxalate-degrading bacteria of the gut microbiome.

Topics: Adult; Bifidobacterium; Calcium; Carboxy-Lyases; Case-Control Studies; Cross-Sectional Studies; Female; Humans; Hyperoxaluria; Kidney Calculi; Lactobacillus; Male; Middle Aged; Oxalates; Oxalobacter formigenes; Recurrence

Oxalate crystal-induced renal inflammation is associated with progressive kidney failure due to activation of the NLRP3/CASP-1 inflammasome. It has been suggested previously that purinergic P2X7 receptor signaling is critical for crystal-induced inflammasome activation and renal injury. Therefore, we investigated the role of the P2X7 receptor in response to crystal-induced cytokine release, inflammation, and kidney failure using in vitro and in vivo models. Dendritic cells and macrophages derived from murine bone marrow and human peripheral blood mononucleated cells stimulated with calcium-oxalate crystals, monosodium urate crystals, or ATP lead to the robust release of interleukin-1beta (IL-1ß). Treatment with the P2X7 inhibitor A740003 or the depletion of ATP by apyrase selectively abrogated ATP-induced, but not oxalate and urate crystal-induced IL-1ß release. In line with this finding, dendritic cells derived from bone marrow (BMDCs) from P2X7

Topics: Adenosine Triphosphate; Animals; Caspase 1; Humans; Interleukin-1beta; Kidney Calculi; Mice; Mice, Inbred C57BL; Oxalates; Purinergic Agonists; Receptors, Purinergic P2X7; Uric Acid

In rats, we recently showed how a chronic metabolic acidosis simultaneously reduced urinary oxalate excretion and promoted oxalate secretion by the distal colon leading to the proposition that acid-base disturbances may trigger changes to renal and intestinal oxalate handling. The present study sought to reproduce and extend these observations using the mouse model, where the availability of targeted gene knockouts (KOs) would offer future opportunities to reveal some of the underlying transporters and mechanisms involved. Mice were provided with a sustained load of acid (NH

Topics: Acetazolamide; Acidosis; Ammonium Chloride; Animals; Carbonic Anhydrase Inhibitors; Carbonic Anhydrases; Disease Models, Animal; Female; Homeostasis; Humans; Intestinal Mucosa; Kidney; Kidney Calculi; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oxalates; Rats; Renal Elimination; Species Specificity

Previous studies have suggested that ω-3 and ω-6 polyunsaturated fatty acid (PUFA) composition in plasma and red blood cell (RBC) total phospholipids plays a role in urolithiasis. Our aim was to test the robustness of this dogma by retrospectively comparing baseline profiles of these parameters in subjects from high- and low-stone-risk groups. The documented difference in stone occurrence in white (relatively common) (W) and black (rare) (B) subjects prompted us to select these groups as the high-low risk model for the study. Blood and urine samples were obtained from ten subjects in each group and were analysed for PUFAs and stone risk factors, respectively. Concentrations of linoleic acid (LA), eicosadienoic acid (EDA) and arachidonic acid (AA) in plasma and or/RBC total phospholipids were significantly higher in B. Differences in other PUFA profiles were also observed. There was no inter-group difference in AA/LA ratios. Urinary oxalate was significantly higher while urinary phosphate was significantly lower in B. We speculate that elevated AA in B might arise because of a possibly enhanced elongation of LA to EDA, as well as an enhanced ∆-8-desaturation of EDA to dihomo-gamma-linolenic acid (DGLA), which is the immediate precursor of AA. Alternatively, we speculate that the ∆-5-desaturation step of DGLA to AA might be more highly activated in this group. Irrespective of the mechanism, our observed inter-group differences in phospholipid PUFA composition are in conflict with previously published dogma which relates PUFA characteristics to high- and low-stone risk.

Topics: Black People; Fatty Acids, Unsaturated; Healthy Volunteers; Humans; Kidney Calculi; Male; Oxalates; Phospholipids; Pilot Projects; Retrospective Studies; Risk Factors; South Africa; White People

Magnesium plays numerous vital roles in human's body. It is known as a protective factor in stone formation by binding to oxalate in the intestinal and urinary system, and decreasing its absorption and crystallization, respectively. Due to controversies about the association between the 24-h urine magnesium and other urine metabolites in different studies, this study was designed to find a clear answer to this question.. In this retrospective cross-sectional study, data from 24-h urinalysis of the calcium stone-forming (CSF) patients were assessed. The correlation between 24-h urine (24-U) magnesium to creatinine ratio (Mg/Cr) with other 24-U metabolites to creatinine ratio was assessed, using Spearman correlation test. The association between 24-U magnesium and 24-U oxalate was also studied in a multivariate logistic regression model.. Among 965 patients, the level of Mg/Cr showed a direct association with all other 24-U metabolite to Cr ratio (p-value < 0.001 for all analyses). The result of multivariate regression analysis showed that the higher quartile of 24-U oxalate (> 47 mg/24 h) increased the odds of 24-U magnesium more than 75 mg/24 h (data median) (OR 1.89, 95% CI 1.14-3.13) comparing with the lower quartile of 24-U oxalate (≤ 26 mg/24 h).. In a routine dietary habit, since rich sources of magnesium contain a high amount of oxalate at the same time, it is not surprising that magnesium level in 24-h urinalysis showed a direct association with 24-h urine oxalate.

Topics: Adult; Calcium; Correlation of Data; Creatinine; Cross-Sectional Studies; Female; Humans; Hydrogen-Ion Concentration; Iran; Kidney; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Renal Elimination; Retrospective Studies; Urinalysis

Green tea is widely used as a ''healthy'' beverage due to its high level of antioxidant polyphenol compounds. However tea is also known to contain significant amount of oxalate. The objective was to determine, in a cross-sectional observational study among a population of 273 hypercalciuric stone-formers referred to our center for metabolic evaluation, whether daily green tea drinkers (

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Citric Acid; Cross-Sectional Studies; Diet; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates; Risk Factors; Tea; Uric Acid; Urinalysis; Young Adult

Treatment targeting osteopontin (OPN) and monocyte chemoattractant protein 1 (MCP‑1) has been recognized as a novel approach in renal crystal formation. The present study was designed to investigate the suppressive effects of metformin on nephrolithiasis formation and its potential mechanism. The cytotoxicity of metformin on MDCK and HK‑2 cells was determined using a Cell Counting Kit‑8 assay in vitro. Subsequently, the mRNA transcription and protein expression levels of MCP‑1 and OPN were detected by reverse transcription‑quantitative‑polymerase chain reaction analysis, western blot analysis and ELISA. Male Sprague‑Dawley rats were divided into a control group, ethylene glycol (EG) group and EG + metformin group. The expression levels of MCP‑1 and OPN and crystal formations were evaluated in renal tissues following an 8‑week treatment period. In vitro, metformin significantly inhibited the production of MCP‑1 and OPN induced by oxalate at the mRNA and protein expression levels. In vivo, increased expression levels of MCP‑1 and OPN were detected in the EG group compared with the controls, and this upregulation was reversed in the EG + metformin group. Renal crystal deposition in the EG + metformin group was markedly decreased compared with that in the EG group. Therefore, the results of the study suggest that metformin suppressed urinary crystal deposit formation, possibly by mediating the expression of inflammatory mediators OPN and MCP‑1.

Topics: Animals; Body Weight; Cell Death; Chemokine CCL2; Disease Models, Animal; Dogs; Ethylene Glycol; Humans; Kidney Calculi; Madin Darby Canine Kidney Cells; Male; Metformin; Osteopontin; Oxalates; Rats, Sprague-Dawley; RNA, Messenger; Up-Regulation

To evaluate the potential of ALLN-177, an orally administered, oxalate-specific enzyme therapy to reduce urine oxalate (UOx) excretion in patients with secondary hyperoxaluria.. Sixteen male and female subjects with both hyperoxaluria and a kidney stone history were enrolled in an open-label study. Subjects continued their usual diets and therapies. During a 3-day baseline period, two 24-h (24-h) urines were collected, followed by a 4-day treatment period with ALLN-177 (7,500 units/meal, 3 × day) when three 24-h urines were collected. The primary endpoint was the change in mean 24-h UOx from baseline. Safety assessments and 24-h dietary recalls were performed throughout.. The study enrolled 5 subjects with enteric hyperoxaluria and 11 with idiopathic hyperoxaluria. ALLN-177 was well tolerated. Overall mean (SD) UOx decreased from 77.7 (55.9) at baseline to 63.7 (40.1) mg/24 h while on ALLN-177 therapy, with the mean reduction of 14 mg/24 h, (95% CI - 23.71, - 4.13). The calcium oxalate-relative urinary supersaturation ratio in the overall population decreased from a mean of 11.3 (5.7) to 8.8 (3.8) (- 2.8; 95% CI - 4.9, - 0.79). This difference was driven by oxalate reduction alone, but not any other urinary parameters. Mean daily dietary oxalate, calcium, and fluid intake recorded by frequent diet recall did not differ by study periods.. ALLN-177 reduced 24-h UOx excretion, and was well tolerated. The results of this pilot study provided justification for further investigation of ALLN-177 in patients with secondary hyperoxaluria.. Clinicaltrials.gov NCT02289755.

Topics: Administration, Oral; Adult; Aged; Carboxy-Lyases; Diet; Enzyme Therapy; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates

Topics: Humans; Kidney Calculi; Oxalates

The pathophysiology of genetic hypercalciuric stone-forming rats parallels that of human idiopathic hypercalciuria. In this model, all animals form calcium phosphate stones. We previously found that chlorthalidone, but not potassium citrate, decreased stone formation in these rats.. To test whether chlorthalidone and potassium citrate combined would reduce calcium phosphate stone formation more than either medication alone, four groups of rats were fed a fixed amount of a normal calcium and phosphorus diet, supplemented with potassium chloride (as control), potassium citrate, chlorthalidone (with potassium chloride to equalize potassium intake), or potassium citrate plus chlorthalidone. We measured urine every 6 weeks and assessed stone formation and bone quality at 18 weeks.. Potassium citrate reduced urine calcium compared with controls, chlorthalidone reduced it further, and potassium citrate plus chlorthalidone reduced it even more. Chlorthalidone increased urine citrate and potassium citrate increased it even more; the combination did not increase it further. Potassium citrate, alone or with chlorthalidone, increased urine calcium phosphate supersaturation, but chlorthalidone did not. All control rats formed stones. Potassium citrate did not alter stone formation. No stones formed with chlorthalidone, and rats given potassium citrate plus chlorthalidone had some stones but fewer than controls. Rats given chlorthalidone with or without potassium citrate had higher bone mineral density and better mechanical properties than controls, whereas those given potassium citrate did not.. In genetic hypercalciuric stone-forming rats, chlorthalidone is superior to potassium citrate alone or combined with chlorthalidone in reducing calcium phosphate stone formation and improving bone quality.

Topics: Animals; Bone Density; Calcium Phosphates; Chlorthalidone; Hypercalciuria; Kidney Calculi; Male; Oxalates; Potassium Citrate; Rats

Intestinal regulation of oxalate absorption is a complex mechanism, not exclusively reliant on the oxalate-degrading anaerobe Oxalobacter formigenes. Using metagenomics, Miller et al. were able to describe a network of bacterial taxa co-occurring with Oxalobacter formigenes in fecal samples from non-stone forming controls and less represented in stone formers. These findings may help to illuminate why previous intervention studies with probiotics have failed to reduce the risk of hyperoxaluria, opening new possibilities for future research.

Topics: Gastrointestinal Microbiome; Homeostasis; Humans; Kidney Calculi; Oxalates; Oxalobacter formigenes; Urinary Calculi

Renal epithelial cell injury is a key step in inducing kidney stone formation. However, research on the role of cell repair in the prevention and treatment of kidney stones is limited. In this study, the repair effect of degraded Porphyra yezoensis polysaccharide (PYP) on oxidative stress-mediated intracellular damage triggered by oxalate in human kidney proximal tubular epithelial (HK-2) cells was investigated, and the influence of molecular weight (Mw) on the repair ability of PYP was elucidated. Polysaccharides with different Mws were prepared by degrading PYP with hydrogen peroxide. Four degraded fractions, namely, PYP1, PYP2, PYP3, and PYP4, were successfully obtained with Mws of 576.2, 49.54, 12.65, and 4.020 kDa, respectively. A damaged cell model was established using 2.6 mmol L-1 oxalate to injure HK-2 cells. Various Mws of PYPs were used to repair the damaged cells. The repair mechanism of PYPs against oxalate-induced oxidative stress was examined by evaluating cell proliferation and physiological function recovery. Our study revealed that PYPs increased the viability of oxalate-injured HK-2 cells and restored their morphological characteristics and cytoskeleton. PYPs reduced the levels of oxalate-mediated lactase dehydrogenase release, reactive oxygen species generation, and intracellular Ca2+, the loss of mitochondrial membrane potential, the number of cells arrested in S phase, the expression of 8-hydroxy-desoxyguanosine and poly ADP ribose polymerase, lysosomal damage, and the number of apoptotic cells. The PYP fraction with low Mw presented an increased repair activity against cellular damage induced by oxalate. The resistance of the repaired renal cells to crystal adhesion and aggregation was stronger than that of the damaged cells. PYPs might inhibit the formation of kidney stones by repairing damaged cells and inhibiting crystal adhesion and aggregation. We concluded that PYP with low Mw could be used as a potential therapeutic agent against renal stone formation and recurrence.

Topics: Acute Kidney Injury; Calcium; Cell Cycle; Cell Line; Cell Survival; Epithelial Cells; Humans; Kidney Calculi; Membrane Potential, Mitochondrial; Molecular Weight; Oxalates; Oxidation-Reduction; Oxidative Stress; Polysaccharides; Porphyra; Reactive Oxygen Species

to study the calcium level in the urine, serum and hairs and to assess the diagnostic value of the calcium level in various biosubstrates in patients with calcium and non-calcium stones.. a total of 99 patients with urinary stone disease were included in the study. A diagnostic value of calcium level in biosubstrates according to the chemical analysis of stone composition performed using qualitative chemical reactions and microcrystalloscopy was evaluated.. Urinary level of calcium and oxalate is proved to have high diagnostic value in patients with calcium nephrolithiasis (specificity 93.9% and 96.9%, and positive predictive value 88.2% and 97.2%, respectively). The specificity and positive predictive value of the calcium level in the hairs was 81.2% and 87.2%, respectively.. A comprehensive study of the elemental spectrum in urine, hair, and serum increases the diagnostic value of the evaluation of calcium, determined by the type of studied biosubstrate and stone type in patients with nephrolithiasis.

Topics: Calcium; Hair; Humans; Kidney Calculi; Oxalates; Urinary Calculi

Higher vitamin B6 intake might reduce urinary excretion of oxalate, one of the major determinants of risk for calcium oxalate kidney stones. Previous studies investigating the association between intake of vitamin B6 and risk of stones found conflicting results. We sought to investigate the association in three large prospective cohorts. We prospectively examined the association in the Health Professionals Follow-up Study (HPFS; n = 42,919 men), Nurses' Health Study I (NHS I; n = 60,003 older women), and Nurses' Health Study II (NHS II; n = 90,629 younger women). Hazard ratios (HRs) and 95% confidence intervals (CIs) for incident stones across categories of total vitamin B6 intake (<3.0, 3.0-4.9, 5.0-9.9, 10.0-39.9, ≥40.0 mg/day) were generated with Cox proportional hazards regression models adjusted for potential confounders. During 3,316,846 person-years of follow-up, 6576 incident kidney stones were confirmed. In univariate and multivariate analyses, there was no association between intake of vitamin B6 and incident stones. The HR for stones in the highest category compared with the lowest was 1.05 (95% CI 0.85, 1.30; p value for trend = 0.61) for HPFS, 0.95 (95% CI 0.76, 1.18; p value for trend = 0.42) for NHS I, and 1.06 (95% CI 0.91, 1.24; p value for trend = 0.34) for NHS II. The pooled adjusted HR for the highest category compared with the lowest was 1.03 (95% CI 0.92, 1.15; p value for trend = 0.60). Intake of vitamin B6 is not associated with risk of incident kidney stones.

Topics: Adult; Aged; Female; Follow-Up Studies; Humans; Incidence; Kidney Calculi; Male; Middle Aged; Oxalates; Proportional Hazards Models; Prospective Studies; Renal Elimination; Risk Assessment; Risk Factors; Vitamin B 6

The association of metabolic syndrome (MetS) traits with urinary calcium (UCE) or oxalate excretion (UOE) is uncertain in calcium stone formers (CSFs). Our aim was to investigate this association in a large group of Caucasian CSFs.. We retrospectively reviewed data of CSFs evaluated at our Kidney Stone Clinic from 1984 to 2015. Data on body mass index (BMI), MetS traits defined according to international consensus, family history of urolithiasis, anti-hypertensive treatments, calcemia, renal function, and 24-h urinary profile of lithogenic risk were collected. The association between MetS traits and UCE or UOE was tested with multivariate linear regression models accounting for a long list of potential confounders.. In a large group of Caucasian CSFs, hypertension was the only MetS trait significantly associated with UCE, while no MetS trait was associated with oxalate excretion.

Topics: Adult; Calcium; Comorbidity; Dyslipidemias; Female; Humans; Hypercalciuria; Hyperoxaluria; Hypertension; Italy; Kidney Calculi; Male; Middle Aged; Overweight; Oxalates; Prevalence; Retrospective Studies

Kidney stones is increasingly associated with obesity. With an increasing prevalence of obesity and metabolic syndrome in the past 30 years, urinary oxalate has significantly increased. However, its underlying pathophysiologic mechanisms of hyperoxaluria have not been fully explored. This preclinical study suggests that hyperoxaluria in obesity depends on a complex network of inflammatory responses linked to metabolic outcome. The future mechanistic and clinical investigations must be targeted at elucidating the pathogenetic role of inflammation in obesity induced hyperoxaluria.

Topics: Humans; Hyperoxaluria; Kidney Calculi; Metabolic Syndrome; Obesity; Oxalates; Prevalence

Primary hyperoxaluria type 3 (PH3) is a recently described cause of childhood renal calculi. It results from mutations in the HOGA1 gene and most cases have been diagnosed after clinical ascertainment, exclusion of other genetic hyperoxalurias and mutation testing. Metabolite testing has not been widely applied but holds promise for the rapid screening and diagnosis of patients who are not specifically suspected to have PH3.. Two cases presented with renal calculi. Urine metabolite testing by tandem mass spectrometry was performed as part of the routine diagnostic work-up for this condition. Both had significantly increased levels of the PH3 urine marker 4-hydroxyglutamate and related metabolites. The diagnosis of PH3 was confirmed by the finding of bi-allelic damaging HOGA1 mutations.. Urine screening by tandem mass spectrometry is a rapid, high-throughput test that can detect PH3 cases that may otherwise not be diagnosed.

Topics: Adolescent; Female; Glutamates; Humans; Hyperoxaluria, Primary; Infant; Ketoglutaric Acids; Kidney Calculi; Lithotripsy; Male; Metabolomics; Oxalates; Oxo-Acid-Lyases; Recurrence; Tandem Mass Spectrometry

Most kidney stones (KS) are composed of calcium oxalate, and small increases in urine oxalate affect the stone risk. Intestinal oxalate secretion mediated by anion exchanger SLC26A6 (PAT1) plays a crucial role in limiting net absorption of ingested oxalate, thereby preventing hyperoxaluria and related KS, reflecting the importance of understanding regulation of intestinal oxalate transport. We previously showed that ATP and UTP inhibit oxalate transport by human intestinal Caco2-BBE cells (C2). Since ATP is rapidly degraded to adenosine (ADO), we examined whether intestinal oxalate transport is regulated by ADO. We measured [

Topics: Adenosine; Adenosine A2 Receptor Antagonists; Adenosine Triphosphate; Amino Acid Transport Systems; Biological Transport; Caco-2 Cells; Humans; Hyperoxaluria; Inflammatory Bowel Diseases; Intestinal Mucosa; Intestines; Kidney Calculi; Oxalates; Receptor, Adenosine A2B; Risk Factors; Signal Transduction; Symporters; Theophylline; Type C Phospholipases

Increased intestinal absorption of oxalate causes hyperoxaluria, a major risk factor for kidney stone disease. Intestinal colonization of recombinant probiotic bacteria expressing oxalate-degrading gene (OxdC) is an effective therapeutic option for recurrent calcium oxalate (CaOx) stone disease. Therefore, we aimed to develop food-grade probiotic L. plantarum secreting OxdC using lactococcal group II intron, Ll.LtrB and evaluate its oxalate degradation ability in vivo. Male Wistar albino rats were divided into four groups. The rats of group I received normal rat chow and drinking water. Groups II, III and IV rats received 5% potassium oxalate containing diet for 28 days. Groups III and IV rats received L. plantarum and food-grade recombinant L. plantarum respectively from 15 to 28 days. Biochemical parameters and crystalluria were analysed in 24 h urine samples. At the end of experimental period, rats were sacrificed; intestine and kidneys were dissected out for colonization studies and histopathological analysis. Herein, we found that the administration of recombinant probiotics significantly reduced the urinary oxalate, calcium, urea, and creatinine levels in rats of group IV compared to group II. Furthermore, colonization studies indicated that recombinant probiotics have gastrointestinal transit and intestinal colonization ability similar to that of wild-type bacteria. In addition, gene expression studies revealed down-regulation of OPN and KIM-1 among group IV rats. Histopathological analysis showed less evidence of nephrocalcinosis in group IV rats. In conclusion, the study demonstrates that food-grade L. plantarum secreting OxdC is capable of degrading intestinal oxalate and thereby prevent CaOx stone formation in experimental rats.

Topics: Alanine Racemase; Animals; Bacterial Proteins; Calcium; Calcium Oxalate; Carboxy-Lyases; Cell Adhesion Molecules; Creatinine; Disease Models, Animal; Gene Expression; Genes, Bacterial; Genomic Instability; Hyperoxaluria; Intestinal Mucosa; Intestines; Introns; Kidney; Kidney Calculi; Lactobacillus plantarum; Male; Mutagenesis; Nephrocalcinosis; Oxalates; Oxalic Acid; Probiotics; Rats; Rats, Wistar; Recombinant Proteins; RNA-Directed DNA Polymerase; Urea

Renal colic is commonly seen in the emergency department (ED), where the focus is on diagnosis and symptom control. Educational materials are sometimes provided upon discharge, however, no standard content has been established. We characterized the educational materials given to patients reporting to EDs in different regions across the U.S. for symptomatic kidney stones, specifically evaluating disease-specific information, symptom management, prevention strategies including dietary recommendations (DRs), and patient follow up plans.. Generic discharge instructions for patients presenting to EDs with renal colic were obtained from community hospitals and academic medical centers between October 2016 and November 2017. Hospitals were called directly. If the same discharge instructions were used by more than one hospital, each was included in our analysis. We assessed the different types of information provided with a focus on stone prevention and DRs by characterizing them into specific nutritional categories.. Of 266 hospitals contacted, 79 provided discharge instructions. Of these, 51 (65%) provided some information on diet. While most recommended higher fluid intake, almost 40% endorsed unnecessary fluid restrictions. Recommendations to reduce protein and oxalate intake were common, but erroneous information for both was given. Nearly 1 in 5 EDs recommended lower calcium intake. Less than 30% of EDs mentioned that stones can have different composition or causes. Less than 30% referenced consultation with a registered dietitian nutritionist (RDN) or that dietary approaches to stone prevention are optimally individualized. Only 9 summaries recommended urologic follow up.. Many ED discharge materials contain DRs for stone prevention. These recommendations can be inaccurate and/or inappropriate. Advice on diet and stone prevention is more appropriately addressed in the outpatient setting when more data (stone composition, serum and urine parameters) and expert consultants are available.

Topics: Calcium; Diet; Dietary Proteins; Dietetics; Drinking; Emergency Service, Hospital; Humans; Kidney Calculi; Oxalates; Patient Discharge; Patient Education as Topic; Referral and Consultation

Hyperoxaluria and oxidative stress are risk factors in calcium oxalate (CaOx) stone formation. Supplement with antioxidant could be effective in prevention of recurrent stone formation. The present study aims to evaluate the protective effects of vitamin E and vitamin C in hyperoxaluric rat. The experiment was performed in rats for 21 days. Rats were divided into 5 groups as follows: control (group 1, n=8), hyperoxaluric rats (group 2, n=8), hyperoxaluric rats with vitamin E supplement (group 3, n=7), hyperoxaluric rats with vitamin C supplement (group 4, n=7) and hyperoxaluric rats with vitamin E and C supplement (group 5, n=7). Hyperoxaluria was induced by feeding hydroxyl L-proline (HLP) 2% w/v dissolved in drinking water. Intraperitoneal 200 mg/kg of vitamin E was given in groups 3 and 5 on days 1, 6, 11 and 16, while 500 mg of vitamin C was injected intravenously in groups 4 and 5 on days 1 and 11. Renal functions and oxidative status were measured. The urinary oxalate excretion was increased in HLP supplement rats, while glomerular filtration rate, proximal water and sodium reabsorption were significantly lower in group 2 compared with a control (P<0.05). Giving antioxidants significantly lower urinary calcium oxalate crystals (P<0.05). Hyperoxaluric rats had higher plasma malondialdehyde (PMDA) and lower urinary total antioxidant status (UTAS), which were alleviated by vitamin E and/or vitamin C supplement. In conclusion, giving combination of vitamin E and vitamin C exerts a protective role against HLP-induced oxalate nephropathy.

Topics: Animals; Antioxidants; Ascorbic Acid; Body Weight; Citrates; Drinking; Drug Therapy, Combination; Eating; Electrolytes; Hemodynamics; Hyperoxaluria; Kidney; Kidney Calculi; Kidney Glomerulus; Male; Oxalates; Protective Agents; Rats; Rats, Sprague-Dawley; Vitamin E

Topics: Child, Preschool; Hematuria; Humans; Hyperoxaluria, Primary; Kidney Calculi; Male; Oxalates; Radiography, Abdominal; Transaminases

Primary Hyperoxaluria type I (PH1) is a rare autosomal recessive disease caused by lack or dysfunction of the liver peroxisomal enzyme alanine: glyoxylate aminotransferase, AGT.. To conduct clinical and genetic characterization of Druze and Muslim Arab patients with PH1 in Northern Israel.. In the last 20 years, 36 children and families were diagnosed and treated in the Nephrology-Genetic Clinic at the Galilee Medical Center. Clinical evaluation for nephrocalcinosis with/without renal stones, elevated excretion of oxalate and glycolate in urine, and genetic workup were performed. Treatment included hemodialysis, and/or peritoneal dialysis. Some patients were directed to preemptive liver transplantation or to combined liver and kidney transplantation. Genetic counseling and prenatal diagnosis were conducted.. Thirty-six patients, from newborns to adults in their 20's, were diagnosed with PH1. They represent 38.8% of patients in the pediatric-dialysis unit. The genetic variant in the AGXT gene causing their disease was identified. Nine prenatal diagnoses were performed, and a genetic screening program was implemented in four Druze villages in the Galilee and Golan Heights.. PH1 is a prevalent disease among Druze and Muslim Arabs in northern Israel. Genetic diagnosis is the gold standard and enables early diagnosis and treatment. Genotype-phenotype correlations are complex. Population screening programs provide an important tool for prevention.. The "genetic islands" of PH1 in northern Israel require a community-based medical approach for the prevention of the disease and the treatment of presymptomatic patients for better prognosis.

Topics: Arabs; Child; Humans; Hyperoxaluria, Primary; Islam; Israel; Kidney Calculi; Mutation; Oxalates; Transaminases

Despite guidelines, routine 24-hour urine testing is completed in <10% of high-risk, recurrent stone formers. Using surrogates for metabolic testing, such as key patient characteristics, could obviate the cost and burden of this test while providing information needed for proper stone prevention counseling.. We performed a retrospective study of 392 consecutive patients from 2007 to 2014 with ≥2 lifetime stone episodes, >70% calcium oxalate by mineral analysis, and ≥1 24-hour urine collection. We compared mean 24-hour urine values by age in decades. We used logistic regression and receiver operating characteristic (ROC) curve analysis to assess the predictive ability of age, gender, body mass index (BMI), and comorbidities to detect abnormal 24-hour urine parameters.. The mean age of the cohort was 51 ± 16 years. Older age was associated with greater urinary oxalate (p-trend <0.001), lower urinary uric acid (UA) (p-trend = 0.007), and lower urinary pH (p-trend <0.001). A nonlinear association was noted between age and urinary calcium or citrate (calcium peaked at 40-49 years, p = 0.03; citrate nadired at 18-29 years, p = 0.001). ROC analysis of age, gender, and BMI to predict 24-hour urine abnormalities performed the best for hyperuricosuria (area under the curve [AUC] 0.816), hyperoxaluria (AUC 0.737), and hypocitraturia (AUC 0.740). Including diabetes mellitus or hypertension did not improve AUC significantly.. In our recurrent calcium oxalate cohort, age significantly impacted urinary calcium, oxalate, citrate, and pH. Along with gender and BMI, age can be used to predict key 24-hour urine stone risk results. These data lay the foundation for a risk prediction tool, which could be a surrogate for 24-hour urine results in recurrent stone formers, who are unwilling or unable to complete metabolic testing. Further validation of these findings is needed in other stone populations.

Topics: Adolescent; Adult; Age Factors; Aged; Body Mass Index; Calcium; Calcium Oxalate; Calcium Phosphates; Citrates; Citric Acid; Comorbidity; Diabetes Mellitus; Female; Humans; Hypercalciuria; Hyperoxaluria; Hypertension; Kidney Calculi; Male; Middle Aged; Nephrolithiasis; Obesity; Oxalates; Recurrence; Regression Analysis; Retrospective Studies; Sex Factors; Uric Acid; Urinalysis; Young Adult

Topics: Calcium Oxalate; HEK293 Cells; Humans; Kidney Calculi; Membrane Potential, Mitochondrial; Oxalates; Oxidative Stress; Reactive Oxygen Species

Topics: Calcium; Calcium Oxalate; Humans; Kidney Calculi; Mitochondria; Monocytes; Oxalates; Urinary Calculi

Hyperoxaluria due to endogenously synthesized and exogenously ingested oxalates is a leading cause of recurrent oxalate stone formations. Even though, humans largely rely on gut microbiota for oxalate homeostasis, hyperoxaluria associated gut microbiota features remain largely unknown. Based on 16S rRNA gene amplicons, targeted metagenomic sequencing of formyl-CoA transferase (frc) gene and qPCR assay, we demonstrate a selective enrichment of Oxalate Metabolizing Bacterial Species (OMBS) in hyperoxaluria condition. Interestingly, higher than usual concentration of oxalate was found inhibitory to many gut microbes, including Oxalobacter formigenes, a well-characterized OMBS. In addition a concomitant enrichment of acid tolerant pathobionts in recurrent stone sufferers is observed. Further, specific enzymes participating in oxalate metabolism are found augmented in stone endures. Additionally, hyperoxaluria driven dysbiosis was found to be associated with oxalate content, stone episodes and colonization pattern of Oxalobacter formigenes. Thus, we rationalize the first in-depth surveillance of OMBS in the human gut and their association with hyperoxaluria. Our findings can be utilized in the treatment of hyperoxaluria associated recurrent stone episodes.

Topics: Bacteria; Case-Control Studies; Dysbiosis; Gastrointestinal Microbiome; Humans; Hyperoxaluria; Kidney Calculi; Male; Metagenomics; Oxalates; Oxalobacter formigenes; Phylogeny; RNA, Ribosomal, 16S; Sequence Analysis, DNA

Oxidative stress is a causal factor and key promoter of urolithiasis associated with renal tubular epithelium cell injury. The present study was designed to investigate the preventive effects of metformin on renal tubular cell injury induced by oxalate and stone formation in a hyperoxaluric rat model. MTT assays were carried out to determine the protection of metformin from oxalate-induced cytotoxicity. The intracellular superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels were measured in vitro. Male Sprague-Dawley rats were divided into control group, ethylene glycol (EG) treated group, and EG + metformin treated group. Oxidative stress and crystal formations were evaluated in renal tissues after 8-week treatment. Metformin significantly inhibited the decrease of the viability in MDCK cells and HK-2 cells induced by oxalate. Besides, metformin markedly prevented the increased concentration of MDA and the decreased tendency of SOD in oxalate-induced MDCK cells and HK-2 cells. In vivo, the increased MDA levels and the reduction of SOD activity were detected in the EG treated group compared with controls, while these parameters reversed in the EG + metformin treated group. Kidney crystal formation in the EG + metformin treated group was decreased significantly compared with the EG treated group. Metformin suppressed urinary crystal deposit formation through renal tubular cell protection and antioxidative effects.

Topics: Animals; Antioxidants; Cell Death; Disease Models, Animal; Dogs; Ethylene Glycol; Humans; Kidney Calculi; Kidney Tubules; Madin Darby Canine Kidney Cells; Male; Malondialdehyde; Metformin; Oxalates; Oxidative Stress; Rats, Sprague-Dawley; Superoxide Dismutase

Urine oxalate measurement is an important investigation in the evaluation of renal stone disease. Primary hyperoxaluria (PH) is a rare inherited metabolic disease characterised by persistently elevated urine oxalate, but the diagnosis may be missed in adults until renal failure has developed. Urine oxalate results were reviewed to compare oxalate:creatinine ratio and oxalate excretion, and to estimate the potential numbers of undiagnosed PH.. Urine oxalate results from August 2011 to April 2013 were reviewed. Oxalate excretion and oxalate:creatinine ratio were evaluated for 24 h collections and ratio alone for spot urine samples.. Oxalate:creatinine ratio and oxalate excretion were moderately correlated (R=0.63) in 24-h urine collections from patients aged 18 years and above. Sex-related differences were found requiring implementation of male and female reference ranges for oxalate:creatinine ratio. Of samples with both ratio and excretion above the reference range, 7% came from patients with confirmed PH. There were 24 patients with grossly elevated urine oxalate who had not been evaluated for PH.. Oxalate:creatinine ratio and oxalate excretion were discordant in many patients, which is likely to be a result of intra-individual variation in creatinine output and imprecision in the collection itself. Some PH patients had urine oxalate within the reference range on occasion, and therefore it is not possible to exclude PH on the finding of a single normal result. A significant number of individuals had urine oxalate results well above the reference range who potentially have undiagnosed PH and are consequently at risk of renal failure.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Case-Control Studies; Child; Child, Preschool; Creatinine; Female; Humans; Hyperoxaluria, Primary; Kidney Calculi; Male; Middle Aged; Oxalates; Reference Values; Referral and Consultation; Sex Factors

To examine the levels of Oxalobacter formigenes in probiotic supplements marketed by PRO-LAB, Ltd, Toronto, Canada, and capsules of Oxalo purchased from Sanzyme Ltd, Hyderabad, India, and to measure the ability of these preparations to degrade oxalate in vitro.. Probiotic supplements and pure cultures of O. formigenes were cultured in a number of media containing oxalate. Optical density at 595 nm (OD595) was used to measure bacterial growth, and ion chromatography was used to measure loss of oxalate in culture media. O. formigenes-specific and degenerate Lactobacillus primers to the oxalate decarboxylase gene (oxc) were used in polymerase chain reaction (PCR).. Incubating probiotic supplements in different media did not result in the growth of oxalate-degrading organisms. PCR indicated the absence of organisms harboring the oxc gene. Culture and 16S ribosomal ribonucleic acid gene sequencing indicated the PRO-LAB supplement contained viable Lactococcus lactis subsp. lactis (GenBank accession no. KJ095656.1), whereas Oxalo contained several Bacillus species and Lactobacillus plantarum.. The probiotic supplement sold over the Internet by PRO-LAB Ltd and Sanzyme Ltd did not contain identifiable O. formigenes or viable oxalate-degrading organisms, and they are unlikely to be of benefit to calcium oxalate kidney stone patients.

Topics: Bacteriological Techniques; Dietary Supplements; Kidney Calculi; Oxalates; Oxalobacter formigenes; Probiotics

Twenty one-year-old local male dogs were randomly assigned into four groups (five dogs per group). The control and the ethylene glycol (EG) groups were fed basal diets without and with EG, and the EG+sodium selenite (EG+SS) and EG+selenium yeast (EG+SY) groups were fed basal diets with EG containing SS and SY, respectively. Blood, urine, and renal samples were taken after 18 weeks of feeding. The results showed that compared with the control group, the serum calcium levels and antioxidase activities significantly decreased in the EG group. Serum creatinine, urea nitrogen, and malondialdehyde (MDA) levels and urine calcium and oxalate levels significantly increased. Calcium oxalate crystal deposition and osteopontin (OPN) messenger RNA and protein expression in the renal tissues significantly increased. These changes above in the EG group were reversed within limits by adding selenium in the diets (both EG+SS and EG+SY groups). Further, compared with the EG+SS group, the EG+SY group showed better effects in decreasing the formation of EG-induced calcium oxalate renal calculi and OPN expression and improving antioxidant capability in dogs. It indicates that organic selenium has the potential value to alleviate the formation of EG-induced calcium oxalate renal calculi.

Topics: Animal Feed; Animals; Antioxidants; Blood Urea Nitrogen; Calcium; Calcium Oxalate; Creatinine; Diet; Dogs; Ethylene Glycol; Kidney Calculi; Male; Malondialdehyde; Osteopontin; Oxalates; Oxidative Stress; Selenium; Urinalysis

There is conflicting evidence about the role of obesity in paediatric nephrolithiasis. This Polish study explored the influence of nutritional status and lipid disturbances on urinary lithogenic factors and the risk of kidney stone formation in children and adolescents from three to 18 years of age.. We carried out serum lipid profile evaluations and 24-h urine chemistry analyses on 493 overweight/obese paediatric participants (mean age 13 years) without nephrolithiasis and 492 healthy normal weight sex and age-matched controls.. A third (33%) of the study group had blood lipid disturbances, with more acidic urine, lower urinary citrate excretion and a higher fraction of ionised calcium and higher Bonn Risk Index than the controls. The participants' body mass index standard deviation score (BMI Z-score) was positively correlated with urinary oxalate and uric acid and negatively correlated with citrate excretion. Total cholesterol, low-density lipoprotein cholesterol and triglycerides correlated negatively with citraturia, while high-density lipoprotein cholesterol correlated positively.. The main factor that predisposed overweight and obese children to kidney stones was hypocitraturia. Urinary citrate excretion was related to both BMI Z-scores and all lipid fraction abnormalities. However, hypercholesterolaemia and particularly low-density lipoprotein hypercholesterolaemia seemed to play a major role.

Topics: Adolescent; Body Mass Index; Calcium; Case-Control Studies; Child; Child, Preschool; Citric Acid; Cross-Sectional Studies; Dyslipidemias; Female; Humans; Kidney Calculi; Male; Nutritional Status; Obesity; Oxalates; Poland; Prospective Studies; Risk Factors; Uric Acid

Topics: Dietary Supplements; Kidney Calculi; Oxalates; Oxalobacter formigenes; Probiotics

Obese patients have an increased risk of kidney stones, and several studies have identified specific urinary derangements on 24-hour collections. The objective of this study was to assess obese and super-obese stone formers, and their compliance with dietary modifications over time, based on 24-hour urine outcomes.. A retrospective review was performed searching for all stone formers who completed a 24-hour urine collection before and after dietary counseling for stone prevention. Patients were excluded if placed on medical therapy in addition to dietary therapy. Patients were divided in three main groups according to their body mass index (BMI): 30, 30-40, and >40 kg/m(2). Demographic data and 24-hour urine stone risk parameters (volume, sodium, uric acid, citrate, and oxalate) were assessed. Initial 24-hour urine results were compared to follow-up results after dietary counseling. Then, the outcomes from each group were compared to each other.. Two hundred and fourteen stone formers (67% male) were identified with a mean age of 49.5±15.0 years. One hundred twenty-eight (59.8%) patients had BMI <30 kg/m(2), 61 (28.5%) between 30-40 kg/m(2), and 25 (11.7%) >40 kg/m(2). Among patients with BMI <30 kg/m(2), there were significant improvements in all urinary parameters (p<0.001) as well as in the group with BMI between 30 to 40 kg/m(2) (p=0.02 for oxalate, p<0.001 for other parameters). Among super-obese patients, there were significant improvements in the urinary volume (p=0.03), sodium (p<0.001), uric acid (p=0.001), and oxalate (p<0.001). There were no significant differences in the improvements observed in the urinary volume (p=0.69), sodium (p=0.08), uric acid (p=0.17), and citrate levels (p=0.97) between the groups.. Dietary recommendations can be an equally effective strategy in decreasing the risk or stone recurrence in obese and super-obese kidney stone formers as it is in those who are not obese.

Topics: Adult; Body Mass Index; Citric Acid; Dietary Supplements; Female; Follow-Up Studies; Humans; Kidney Calculi; Male; Middle Aged; Obesity; Oxalates; Retrospective Studies; Sodium; Uric Acid

Distinguishing calcium oxalate from uric acid stones is critical to identify those patients who may benefit from dissolution therapy and can also help direct preventive measures for stone growth. We aim to study whether 24-hour urine analysis may predict the urinary stone composition.. We retrospectively identified patients with calcium oxalate and uric acid stone compositions who also had a 24-hour urine collection within 3 months of stone analysis. Patients with calcium phosphate, cystine, and other stone compositions were excluded. Subjects were divided based on their stone type (calcium oxalate vs uric acid stones) and were compared according to demographic data and 24-hour urine analysis. Logistic regression analysis was performed to assess the association between stone composition and covariates. A nomogram was then constructed to predict uric acid stones over calcium oxalate stones.. Of the 1163 patients identified, 1054 (90.6%) had calcium oxalate stones and 109 (9.4%) had uric acid stones. On logistic regression, body mass index (BMI) (odds ratio [OR] 1.351, 95% confidence interval [CI] 1.133-1.609; P<0.001), urinary sodium (OR 1.021, 95% CI 1.004-1.037; P=0.013), calcium (OR 0.987, 95% CI 0.979-0.996; P=0.003), oxalate (OR 0.890, 95% CI 0.804-0.985; P=0.024), and uric acid (OR 0.989, 95% CI 0.982-0.997; P=0.005) were significant predictors for urinary stone composition. The nomogram with the highest concordance index (c-index=0.855) was obtained using age, BMI, urinary sodium, calcium, oxalate, and uric acid as variables.. Distinguishing uric acid from calcium oxalate stones can be performed with relative accuracy using parameters from the 24-hour urine stone risk profile and the patient's BMI and age.

Topics: Body Mass Index; Calcium; Calcium Oxalate; Diagnosis, Differential; Female; Humans; Kidney Calculi; Male; Middle Aged; Nephrolithiasis; Nomograms; Oxalates; Predictive Value of Tests; Regression Analysis; Retrospective Studies; Sodium; Time Factors; Uric Acid

This work aimed to underline the prospects of hippuric acid, a product of the metabolism of polyphenols, as a new biomarker of fruits and vegetables intake associated with lithogenic risk. Biochemical parameters of lithogenic risk and hippuric acid were measured in the 24 h urine collections of a cohort of 696 Italian kidney stone formers divided into two subgroups according to their different dietary habits. The link between lithogenic risk parameters and hippuric acid was assessed and this compound was revealed as a valuable biomarker of fruits and vegetables intake in kidney stone formers. A cut-off value of urinary excretion of hippuric acid, 300 mg/24 h, was set as the threshold of discrimination between low and high intake of fruits and vegetables for these patients. These results highlight the importance of monitoring of the excretion hippuric acid in urine to address proper dietary guidelines for the management of stone former patients.

Topics: Adolescent; Adult; Biomarkers; Calcium; Diet; Feeding Behavior; Female; Fruit; Hippurates; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Plant Extracts; Polyphenols; Urine Specimen Collection; Vegetables; Young Adult

To evaluate the trends in the American diet over the last 40 years (1974-2010), during which time the National Health and Nutrition Examination Survey data set has documented an increase in stone prevalence from 3.8% to 8.8%.. We used the National Health and Nutrition Examination Survey reported rates for stone disease (1974-2010) to compare the United States Department of Agriculture's food distribution data during the same period. Three data points for prevalence were used from the literature. We correlated these to changing lithogenic food distributions using linear models to interpolate annual changes in prevalence. Spearman correlations were performed (P ≤.05) using SAS 9.2 (SAS Institute, Cary, NC).. Increased total daily calories (rho, 0.96; P <.001), fat (rho, 0.79; P <.001), protein (rho, 0.85; P <.001), fruit (rho, 0.6; P = .01), and vegetables (rho, 0.73; P <.001) correlated strongly with increasing stone prevalence. Dark green vegetables, flour or cereal products, fish or shellfish, corn products (including high fructose corn syrup), and added sugars also showed strong correlations with stone prevalence. Citrus fruits were negatively correlated to stone disease (rho, -0.18; P = .31). Protein, fruits and vegetables, and added sugars actually decreased in proportion to daily caloric per capita increases.. Increases in caloric intake and several lithogenic foods correlate temporally with increasing stone prevalence. The nature of this relationship is difficult to determine from this data; although, clearly, American diets have changed over the last 4 decades.

Topics: Dairy Products; Diet; Dietary Proteins; Energy Intake; Feeding Behavior; Fish Products; Fruit; Humans; Kidney Calculi; Nutrition Surveys; Oxalates; Prevalence; Purines; United States; Vegetables

Topics: Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Oxalates

Helicobacter pylori (H. pylori) is a atypical gram-negative bacteria preferring gastric mucosa which also have bizarre multisystem effects extended to some malignancies, hematologic and vascular disorders through some not well defined pathophysiologic pathways. Our pioneer data was pointing that the urinary system stone existence was seemed to be high in the group of H. pylori+cases. While the explanation of the reason of the coincidence of renal-gall bladder stones, it was previously suggested that there may be a shift mechanism of intestinal microbial flora, from Oxalobacter formigenes that may reduce the risk of renal stone by consuming intestinal oxalate, to H. pylori which is known to induce gallstone by unknown mechanism. This hypothesis is an indirect one and highly controversial for the effect of H. pylori in the renal stone formation because intestinal absorption of oxalate is not significant when it is compared with the endogen oxalate. The present preliminary unique data in connection with our hypothesis claimed that a possible relation between H. pylori and renal stones. We think that this detrimental effect is due to the possible systemic influence such as vascular and/or endoluminal sickness due to the H. pylori other than directs bacteriologic colonization. There is strong evidence that H. pylori have some role in the atherosclerotic procedure. The vascular theory of Randall plaque formation at renal papilla and subsequent calcium oxalate stone development that suggests microvascular injury of renal papilla in an atherosclerotic-like fashion results in calcification near vessel walls that eventually erodes as a calculus format into the urinary system. Briefly, theories of stone and atherosclerosis seemed to be overlap and H. pylori is one of the factor of both processes. In addition to our hypothesis, we claimed that H. pylori might have same detrimental effect on endoluminal surfaces of urinary and genital systems and resulting in some special pathologies as Hunner's ulcers in interstitial cystitis and even posttesticular infertility. The accumulating knowledge about extragastric sequelae of H. pylori may open new aspects on therapeutic and the prevention strategies of urolithiasis and even this progress may reach to chronic pelvic pain syndromes and idiopathic infertility.

Topics: Apoptosis; Atherosclerosis; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Absorption; Intestines; Kidney Calculi; Models, Theoretical; Oxalates; Oxalobacter formigenes; Urinary Calculi; Urolithiasis

The combination of hyperoxaluria and hypocitraturia can trigger Ca(2+)-oxalate stone formation, even in the absence of hypercalciuria, but the molecular mechanisms that control urinary oxalate and citrate levels are not understood completely. Here, we examined the relationship between the oxalate transporter SLC26A6 and the citrate transporter NaDC-1 in citrate and oxalate homeostasis. Compared with wild-type mice, Slc26a6-null mice exhibited increased renal and intestinal sodium-dependent succinate uptake, as well as urinary hyperoxaluria and hypocitraturia, but no change in urinary pH, indicating enhanced transport activity of NaDC-1. When co-expressed in Xenopus oocytes, NaDC-1 enhanced Slc26a6 transport activity. In contrast, Slc26a6 inhibited NaDC-1 transport activity in an activity dependent manner to restricted tubular citrate absorption. Biochemical and physiologic analysis revealed that the STAS domain of Slc26a6 and the first intracellular loop of NaDC-1 mediated both the physical and functional interactions of these transporters. These findings reveal a molecular pathway that senses and tightly regulates oxalate and citrate levels and may control Ca(2+)-oxalate stone formation.

Topics: Animals; Antiporters; Citrates; Dicarboxylic Acid Transporters; Female; Homeostasis; Intestinal Mucosa; Kidney; Kidney Calculi; Mice; Mice, Knockout; Organic Anion Transporters, Sodium-Dependent; Oxalates; Protein Structure, Tertiary; Sulfate Transporters; Symporters; Xenopus

To assess the efficacy of dietary management for the treatment of idiopathic hyperoxaluria in a large tertiary care center and examine the influence of patient factors, compliance, and follow-up on oxalate reduction, which has not been previously investigated.. Retrospectively, 149 patients with kidney stones with idiopathic hyperoxaluria who received dietary management at our stone clinic were evaluated. Changes in urinary parameters on 24-hour urine collections were calculated for all patients and those with abnormal values in the overall short-term (30-240 days) and long-term (>240 days) time periods. Changes in urinary oxalate were evaluated with respect to patient characteristics and compliance measures.. Urine oxalate and supersaturation of calcium oxalate were significantly (P < .001) reduced by 8.9 ± 19.2 mg/d and 1.7 ± 4.3, respectively. A total of 48.3% of the patients reduced their urinary oxalate to normal. Urine oxalate reductions were similar in the short-term and long-term periods. Women lowered urine oxalate nearly twice as much as men (12.7 ± 2.0 mg/d vs 6.7 ± 2.2 mg/d, P = .022) and body mass index (BMI) negatively correlated with oxalate reduction (Pearson's r = -0.213). Reported noncompliance and keeping follow-up appointments did not affect oxalate, however, there was a significant correlation between increasing urine volume and reducing oxalate (Pearson's r = -0.21).. This study confirms that meaningful reductions of urine oxalate and supersaturation of calcium oxalate can be achieved with dietary management of hyperoxaluria on a larger clinical scale. Furthermore, we identified that women and patients with low BMIs had greater urine oxalate reductions and urine volume may also be used by clinicians as a measure of dietary compliance.

Topics: Adult; Body Mass Index; Calcium Oxalate; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates; Patient Compliance; Retrospective Studies; Treatment Outcome

The sequence of events by which primary hyperoxaluria type 1 (PH1) causes renal failure is unclear. We hypothesize that proximal tubule (PT) is vulnerable because oxalate secretion raises calcium oxalate (CaOx) supersaturation (SS) there, leading to crystal formation and cellular injury. We studied cortical and papillary biopsies from two PH1 patients with preserved renal function, and seven native kidneys removed from four patients at the time of transplant, after short-term (2) or longer term (2) dialysis. In these patients, and another five PH1 patients without renal failure, we calculated oxalate secretion, and estimated PT CaOx SS. Plasma oxalate was elevated in all PH1 patients and inverse to creatinine clearance. Renal secretion of oxalate was present in all PH1 but rare in controls. PT CaOx SS was >1 in all nonpyridoxine-responsive PH1 before transplant and most marked in patients who developed end stage renal disease (ESRD). PT from PH1 with preserved renal function had birefringent crystals, confirming the presence of CaOx SS, but had no evidence of cortical inflammation or scarring by histopathology or hyaluronan staining. PH1 with short ESRD showed CaOx deposition and hyaluronan staining particularly at the corticomedullary junction in distal PT while cortical collecting ducts were spared. Longer ESRD showed widespread cortical CaOx, and in both groups papillary tissue had marked intratubular CaOx deposits and fibrosis. CaOx SS in PT causes CaOx crystal formation, and CaOx deposition in distal PT appears to be associated with ESRD. Minimizing PT CaOx SS may be important for preserving renal function in PH1.

Topics: Adolescent; Adult; Biopsy; Calcium Oxalate; Child, Preschool; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Infant; Kidney Calculi; Male; Oxalates; Renal Insufficiency

Certain dietary modifications limit the risk of stone recurrence. Compliance is an important component of dietary therapy for stone prevention, and self-efficacy is an important ingredient of compliance. We developed an internet program to facilitate dietary compliance for stone prevention and performed a pilot study to assess its effectiveness.. The internet program provides information regarding dietary modifications including increased fluid consumption, limited animal protein, sodium, and oxalate intake, and adequate calcium consumption. Participants record their daily food and fluid intake and receive immediate feedback as to whether they were compliant or not. Five adult calcium stone formers collected three 24 hour urine specimens on self-selected diets, three 24 hour urine specimens while on a stone preventive metabolic diet, and three 24 hour urine specimens after utilizing the internet program for 1 month. Urinary stone risk parameters were measured, and data were analyzed using repeated measures ANOVA and Student's t test.. All participants recorded their meals and snacks for each day and found the program easy to navigate. The mean time in hours from food consumption to log in was 35.25 +/- 70.8 hours. There were no statistically significant differences in stone risk factors between the controlled and internet dietary phases. Oxalate excretion was significantly higher during the self-selected dietary intake (p = 0.03).. This pilot study demonstrates that subjects appear to be compliant with utilization of an interactive internet program for stone prevention with dietary modifications. In addition, improvement in certain stone risk parameters occurred.

Topics: Adult; Diet Records; Feasibility Studies; Feeding Behavior; Female; Humans; Internet; Kidney Calculi; Male; Middle Aged; Oxalates; Patient Compliance; Patient Education as Topic; Pilot Projects; Risk Factors; Self Care; Software

The development of effective preventive therapy for renal calculi in patients with secondary hyperoxaluria (2°HO) relies on establishing the pattern of normal variation in urinary oxalate (uOx) and attempting to reduce it. Therefore, we evaluated uOx at baseline and at subsequent time points in stone formers with 2°HO.. We reviewed the charts of 201 recurrent stone formers with 2°HO (uOx ≥ 40 mg/day). The 24-hour urine collections at baseline and after initiation of clinician-directed therapies were analyzed. Mixed models were constructed to analyze uOx over time for individual patients and as a group. Subgroup analyses were performed for enteric and idiopathic 2°HO. Coefficients of variation were computed using the root mean square error from linear models.. The etiology of 2°HO was enteric in 17.9% and idiopathic in 82.1% of patients. Among the 943 urine collections analyzed, 196 oxalate values were derived from the enteric group and 747 from the idiopathic group. The median number of uOx values measured per person was four. The median 24-hour uOx (mg/day) was significantly higher for the enteric group than for the idiopathic group at the time of diagnosis: 64.4 (interquartile range [IQR]=48-90) vs 46.0 (IQR=38-56), P<0.001) and during follow-up (58.2 [IQR=46-86] vs 44.2 [IQR=35-53], P<0.001). Over a median follow-up of 22.5 months, 44.4% of the enteric and 61.8% of the idiopathic patients had at least one normal uOx value (P=0.06). The coefficients of variation for the enteric and idiopathic groups were 40.8% and 27.3%, respectively, with variation randomly displayed in either direction for both groups.. Among patients with 2°HO, uOx demonstrates significant random variation over time even with the incorporation of standard treatments, with enteric HO demonstrating higher values and greater variance than idiopathic HO.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Diagnosis, Differential; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates; Prognosis; Retrospective Studies; Young Adult

Hyperoxaluria is one of etiologic factors of calcium oxalate kidney stone disease. However, response of renal tubular cells to high-oxalate environment remained largely unknown. We applied a gel-based proteomics approach to characterize changes in cellular proteome of MDCK cells induced by 10mM sodium oxalate. A total of 14 proteins were detected as differentially expressed proteins. The oxalate-induced up-regulation of alpha-enolase in whole cell lysate was confirmed by 2-D Western blot analysis. Interaction network analysis revealed that cellular adaptive response under high-oxalate condition involved stress response, energy production, metabolism and transcriptional regulation. Down-regulation of RhoA, which was predicted to be associated with the identified proteins, was confirmed by immunoblotting. In addition, the up-regulation of alpha-enolase on apical surface of renal tubular epithelial cells was also confirmed by immunoblotting of the isolated apical membranes and immunofluorescence study. Interestingly, blockage of alpha-enolase expressed on the cell surface by antibody neutralization significantly reduced the number of calcium oxalate monohydrate (COM) crystals adhered on the cells. These results strongly suggest that surface alpha-enolase plays an important role as the enhancer of COM crystal binding. The increase of alpha-enolase expressed on the cell surface may aggravate kidney stone formation in patients with hyperoxaluria.

Topics: Animals; Calcium Oxalate; Cell Membrane; Crystallization; Dogs; Down-Regulation; Electrophoresis, Gel, Two-Dimensional; Hyperoxaluria; Kidney Calculi; Kidney Tubules; Madin Darby Canine Kidney Cells; Microscopy, Confocal; Microscopy, Fluorescence; Oxalates; Oxalic Acid; Phosphopyruvate Hydratase; Proteins; Proteomics; rhoA GTP-Binding Protein; Tandem Mass Spectrometry

The relationship between diet and the formation of renal stones is demonstrated, but restrictive diets do not take into account the complexity of metabolism and the complex mechanisms that regulate the saturation and crystallization processes in the urine. The restriction of dietary calcium can reduce the urinary excretion of calcium but severe dietary restriction of calcium causes hyperoxaluria and a progressive loss of bone mineral component. Furthermore urinary calcium excretion is influenced by other nutrients than calcium as sodium, potassium, protein and refined carbohydrates. Up to 40% of the daily excretion of oxalate in the urine is from dietary source, but oxalate absorption in the intestine depends linearly on the concomitant dietary intake of calcium and is influenced by the bacterial degradation by several bacterial species of intestinal flora. A more rational approach should be based on the cumulative effects of foods and different dietary patterns on urinary saturation rather than on the effect of single nutrients. A diet based on a adequate intake of calcium (1000-1200 mg per day) and containment of animal protein and salt can decrease significantly urinary supersaturation for calcium oxalate and reduce the relative risk of stone recurrence in hypercalciuric renal stone formers. The DASH-style diet that is high in fruits and vegetables, moderate in low-fat dairy products and low in animal proteins and salt is associated with a lower relative supersaturation for calcium oxalate and a marked decrease in risk of incident stone formation. All the diets above mentioned have as a common characteristic the reduction of the potential acid load of the diet that can be correlated with a higher risk of recurrent nephrolithiasis, because the acid load of diet is inversely related to urinary citrate excretion. The restriction of protein and salt with an adequate calcium intake seem to be advisable but should be implemented with the advice to increase the intake of vegetables that can carry a plentiful supply of alkali that counteract the acid load coming from animal protein. New prospective studies to evaluate the effectiveness of the diet for the prevention of renal stones should be oriented to simple dietary advices that should be focused on a few specific goals easily controlled by means of self-evaluation tools, such as the LAKE food screener.

Topics: Acids; Beverages; Calcium; Calcium Oxalate; Calcium, Dietary; Diet; Dietary Proteins; Drinking Water; Fruit; Humans; Hyperoxaluria; Kidney Calculi; Oxalates; Patient Education as Topic; Secondary Prevention; Sodium, Dietary; Vegetables

Homoscedasticity (constant variance over axes or among statistical factors) is an integral assumption of most statistical analyses. However, a number of empirical studies in model organisms and humans demonstrate significant differences in residual variance (that component of phenotype unexplained by known factors) or intra-individual variation among genotypes. Our work suggests that renal traits may be particularly susceptible to randomization by genetic and non-genetic factors, including endogenous variables like age and weight.. We tested associations between age, weight and intra-individual variation in urinary calcium, citrate, chloride, creatinine, potassium, magnesium, sodium, ammonium, oxalate, phosphorus, sulfate, uric acid and urea nitrogen in 9,024 male and 6,758 female kidney stone patients. Coefficients of variation (CVs) were calculated for each individual for each solute from paired 24-hour urines. Analysis of CVs was corrected for inter-measurement collection variance in creatinine and urine volume. CVs for sodium and urea nitrogen were included to correct for dietary salt and protein.. Age was positively associated with individual CVs for calcium and negatively associated with CVs for potassium, ammonium and phosphorus (p(FDR) < 0.01). Weight was associated with CVs for creatinine, magnesium and uric acid, and negatively associated with CVs for calcium, potassium and oxalate (p(FDR) < 0.05).. Intra-individual variation changes over age and weight axes for numerous urinary solutes. Changing residual variance over age and weight could cause bias in the detection or estimation of genetic or environmental effects. New methodologies may need to account for such residual unpredictability, especially in diverse collections.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Body Weight; Calcium; Chlorides; Citrates; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphorus; Potassium; Quaternary Ammonium Compounds; Sodium; Sulfates; Uric Acid; Urinalysis; Young Adult

The traditional use of Punica granatum has been reported to regulate urine discharge and controls the burning sensation of urine.. Animals model of calcium oxalate urolithiasis was developed in male rats by adding ethylene glycol 0.75% in drinking water. The Punica granatum chloroform extract (PGCE) and Punica grantum methanol extract (PGME) orally at 100, 200 and 400mg/kg, respectively, were administered along with ethylene glycol for 28 days. On 28 day, 24h urine was collected from individual rats and used for estimation of urine calcium, phosphate and oxalate. The serum creatinine, urea and uric acid levels were estimated in each animal. The kidney homogenate was used for the estimation of renal oxalate contents. The paraffin kidney sections were prepared to observe the CaOx deposits.. The ethylene glycol control (Gr.-II) had significant (P<0.001 vs. normal) increase in levels of urine oxalate, calcium and phosphate, serum creatinine, urea and uric acid and renal tissues oxalates, as compared to normal (Gr.-I). The paraffin kidney sections show significant histopathological changes. The treatment of PGCE and PGME at 100, 200 and 400mg/kg doses, significantly (P<0.001 vs. control) decreased the urine oxalate, calcium and phosphate, renal tissue oxalates and serum creatinine, urea and uric acid, in EG induced urolithiasis after 28 days.. The PGCE and PGME at the doses of 400mg/kg, found to be more effective in decreasing the urolithiasis and regeneration of renal tissues in male rats.

Topics: Animals; Calcium; Calcium Oxalate; Creatinine; Ethylene Glycol; Kidney; Kidney Calculi; Lythraceae; Male; Oxalates; Phosphates; Phytotherapy; Plant Extracts; Rats; Rats, Wistar; Urea; Uric Acid; Urolithiasis

Oxalate-binding proteins are thought to serve as potential modulators of kidney stone formation. However, only few oxalate-binding proteins have been identified from previous studies. Our present study, therefore, aimed for large-scale identification of oxalate-binding proteins in porcine kidney using an oxalate-affinity column containing oxalate-conjugated EAH Sepharose 4B beads for purification followed by two-dimensional gel electrophoresis (2-DE) to resolve the recovered proteins. Comparing with those obtained from the controlled column containing uncoupled EAH-Sepharose 4B (to subtract the background of non-specific bindings), a total of 38 protein spots were defined as oxalate-binding proteins. These protein spots were successfully identified by quadrupole time-of-flight mass spectrometry (MS) and/or tandem MS (MS/MS) as 26 unique proteins, including several nuclear proteins, mitochondrial proteins, oxidative stress regulatory proteins, metabolic enzymes and others. Identification of oxalate-binding domain using the PRATT tool revealed "L-x(3,5)-R-x(2)-[AGILPV]" as a functional domain responsible for oxalate-binding in 25 of 26 (96%) unique identified proteins. We report herein, for the first time, large-scale identification and characterizations of oxalate-binding proteins in the kidney. The presence of positively charged arginine residue in the middle of this functional domain suggested its significance for binding to the negatively charged oxalate. These data will enhance future stone research, particularly on stone modulators.

Topics: Animals; Chromatography, Affinity; Kidney; Kidney Calculi; Mass Spectrometry; Oxalates; Protein Binding; Protein Structure, Tertiary; Proteins; Swine

An analytical method for the determination of the composition of renal stones by capillary isotachophoresis with conductometric detection was developed. Using different leading/terminating electrolyte systems, the qualitative and quantitative analysis of organic compounds (urate, xanthate, oxalate) and inorganic ions (phosphate, Ca(2+), Mg(2+), Na(+), NH(4)(+)) species commonly present in mixed renal stones in three separate steps can be carried out with limits of detection about 10 μmol/L. The developed method was validated by the analysis of real samples and can be used for urinary calculi classification. In addition, it was verified that this method can also be employed for the determination of the above mentioned analytes in some other samples (bones, teeth) concerning apatite biominerals (fluoro-, carbonate-, chloro-apatite).

Topics: Anions; Apatites; Bone and Bones; Carbonates; Cations, Divalent; Cations, Monovalent; Conductometry; Humans; Isotachophoresis; Kidney Calculi; Limit of Detection; Oxalates; Phosphates; Salts; Tooth; Uric Acid

The aim of this study is to investigate the serum levels of parathyroid hormone (PTH), calcitonin, 1,25 (OH)(2) vitamin D3, estradiol and testosterone in male patients with active renal calcium stone disease compared with controls and investigate their relationship with serum/urinary biochemistry. Male active renal calcium stone formers (ASF) were enrolled from December 2008 to April 2009. Controls were selected from age and sex matched individuals. Two 24-h urine samples and a blood sample were withdrawn from each participant while they were on free diet. Serum 1,25 (OH)(2) vitamin D3 levels in the ASF and control groups were 127 ± 40 and 93 ± 35 pmol/l (p < 0.001). Serum levels of PTH, calcitonin, estradiol and testosterone were not statistically different between the ASF and control groups (all p > 0.05). Serum 1,25 (OH)(2) vitamin D3 was associated with higher urinary excretion of calcium and phosphorus in ASF patients. Serum levels of calcitonin were related to less urinary excretion of calcium in the control group. Serum testosterone was related to higher urinary excretion of uric acid in ASF patients and to higher urinary excretion of oxalate in the control group. 1,25 (OH)(2) Vitamin D3 is an important hormone in the pathogenesis of recurrent renal calcium stone disease and could increase renal stone risk by increasing the urinary excretion of calcium and phosphorus. There is a possibility of testosterone involvement in the pathogenesis of renal stones through higher urinary uric acid and oxalate excretion.

Topics: Adult; Calcitonin; Calcitriol; Calcium; Estradiol; Hormones; Humans; Immunoenzyme Techniques; Kidney Calculi; Male; Middle Aged; Oxalates; Parathyroid Hormone; Phosphates; Retrospective Studies; Testosterone; Uric Acid

Little is known about the renal handling of oxalate in patients with idiopathic hypercalciuria (IH). To explore the role of tubular oxalate handling in IH and to evaluate whether differences exist between IH and normal controls, we studied 19 IH subjects, 8 normal subjects, and 2 bariatric stone formers (BSF) during a 1-day General Clinical Research Center protocol utilizing a low-oxalate diet. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, oxalate, and calories. Plasma oxalate concentrations and oxalate-filtered loads were similar between patients (includes IH and BSF) and controls in both the fasting and fed states. Urinary oxalate excretion was significantly higher in patients vs. controls regardless of feeding state. Fractional excretion of oxalate (FEOx) was >1, suggesting tubular secretion of oxalate, in 6 of 19 IH and both BSF, compared with none of the controls (P < 0.00001). Adjusted for water extraction along the nephron, urine oxalate rose more rapidly among patients than normal subjects with increases in plasma oxalate. Our findings identify tubular secretion of oxalate as a key mediator of hyperoxaluria in calcium stone formers, potentially as a means of maintaining plasma oxalate in a tight range.

Topics: Adult; Calcium; Diet; Female; Humans; Hypercalciuria; Kidney Calculi; Kidney Tubules; Male; Middle Aged; Oxalates

Enteric colonization with Oxalobacter formigenes, a bacterium whose main energy source is oxalate, has been demonstrated to decrease the risk of recurrent calcium oxalate kidney stone formation. We assessed the impact of diets controlled in calcium and oxalate contents on urinary and fecal analytes in healthy subjects who were naturally colonized with O. formigenes or not colonized with O. formigenes.. A total of 11 O. formigenes colonized and 11 noncolonized subjects were administered diets controlled in calcium and oxalate contents. We assayed 24-hour urine collections and stool samples obtained on the last 4 days of each 1-week diet for stone risk parameters and O. formigenes levels. Mixed model analysis was used to determine the effects of colonization status on these variables.. Urinary calcium and oxalate excretion were significantly altered by the dietary changes in O. formigenes colonized and noncolonized individuals. Mixed model analysis showed significant interaction between colonization status and oxalate excretion on a low calcium (400 mg daily)/moderate oxalate (250 mg daily) diet (p = 0.026). Urinary oxalate excretion was 19.5% lower in O. formigenes colonized subjects than in noncolonized subjects on the low calcium/moderate oxalate diet (mean ± SE 34.9 ± 2.6 vs 43.6 ± 2.6 mg, p = 0.031).. Results suggest that O. formigenes colonization decreases oxalate excretion during periods of low calcium and moderate oxalate intake.

Topics: Adult; Biological Therapy; Calcium, Dietary; Feces; Female; Humans; Kidney Calculi; Male; Oxalates; Oxalobacter formigenes

Seven common marmoset monkeys (Callithrix jacchus) from a laboratory colony of 17 died over a period of eight months. Death of six of these monkeys was attributed to kidney failure from an oxalate-induced nephropathy. The epidemiology of this outbreak suggested an exogenous source and there was strong evidence that the source was bark and leaves from an Eucalyptus viminalis tree. Branches of this tree were introduced one month before the first death. The branches were removed one month after deaths commenced, but deaths continued for another five months. Urinalysis of all surviving marmosets at 80 and 122 days after initial contact with the E viminalis branches suggested that these monkeys had renal impairment. In the cases described here, the eating behaviour of common marmosets apparently exposed the animals to toxic levels of oxalate in the bark and leaves of an E viminalis tree.

Topics: Animal Husbandry; Animals; Animals, Laboratory; Callithrix; Eucalyptus; Fatal Outcome; Female; Kidney Calculi; Kidney Diseases; Male; Monkey Diseases; Oxalates; Plant Poisoning

Topics: Animals; Fatal Outcome; Female; Kidney Calculi; Kidney Diseases; Male; Oxalates; Sex Factors; Sheep; Sheep Diseases

Topics: Female; Humans; Hypercalciuria; Kidney Calculi; Kidney Tubules; Male; Oxalates

Exposure to high levels of oxalate and calcium oxalate monohydrate (COM) crystals is injurious to renal epithelial cells and triggers serial responses related to stone formation. Multiple molecules and proteins are involved in this process, but previous studies have generally been limited, without an overall understanding of protein expression alteration after oxalate and/or crystal exposure as well as its role in stone formation. We used proteomic analysis to reveal the changes in the proteome of HK-2 cells induced by oxalate and COM crystals, so as to provide candidate proteins involved in the molecular mechanisms concerning HK-2 cell injury and kidney stone formation. HK-2 cells were exposed to oxalate plus COM crystals at different concentrations in various samples. Cell viability was determined using a Cell Counting Kit-8 assay kit. For proteomic analysis, cells were exposed to oxalate (2 mM) and COM crystals (200 ug/ml) for 12 h. The proteins were separated by two-dimensional electrophoresis and the differentially expressed proteins were identified by liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS). Validation of protein expression was further performed by Western blot analysis. Oxalate and COM crystals showed concentration-dependent toxicity on HK-2 cells. A total of 12 differentially expressed proteins in HK-2 cells induced by oxalate and COM crystals were identified, which were involved in various aspects of cellular processes. Our study provides a platform for further studying the molecular mechanism of renal epithelial cell injury and kidney stone formation.

Topics: Calcium Oxalate; Cells, Cultured; Crystallization; Epithelial Cells; Humans; Kidney Calculi; Kidney Tubules, Proximal; Oxalates; Proteomics; Renal Insufficiency

Teas prepared from the fruits of Ammi visnaga L. (syn. "Khella") have been traditionally used in Egypt as a remedy to treat kidney stones. It was the aim of our study to evaluate the effect of a Khella extract (KE) as well as the two major constituents khellin and visnagin on renal epithelial injury using LLC-PK1 and Madin-Darby-canine kidney (MDCK) cells. Both cell lines provide suitable model systems to study cellular processes that are possibly involved in the development of a renal stone. LLC-PK1 and MDCK cell lines were exposed to 300 microM oxalate (Ox) or 133 microg/cm(2) calcium oxalate monohydrate (COM) in presence or absence of 10, 50, 100 or 200 microg/mL KE. To evaluate cell damage, cell viability was assessed by determining the release of lactate dehydrogenase (LDH). KE (e.g. 100 microg/ml) significantly decreased LDH release from LLC-PK1 (Ox: 8.46+0.76%; Ox + 100 microg/ml KE: 5.41+0.94%, p<0.001) as well as MDCK cells (Ox: 30.9+6.58%; Ox+100 microg/ml KE: 17.5+2.50%, p<0.001), which indicated a prevention of cell damage. Similar effects for KE were observed in both cell lines when COM crystals were added. In LLC-PK1 cells khellin and visnagin both decreased the % LDH release significantly in cells that were pretreated with Ox or COM crystals. However, khellin and visnagin exhibited different responses in MDCK cells. Whereas khellin slightly reduced the % LDH release after exposure of the cells to Ox and COM crystals, visnagin significantly decreased % LDH release only after COM crystal exposure. Overall both compounds were more active in LLC-PK1 than in MDCK cells. In summary, exposure of renal epithelial cells to Ox or COM crystals was associated with a significant release of LDH indicating cell injury. Our data demonstrate that KE as well as khellin and visnagin could prevent renal epithelial cell damage caused by Ox and COM and could therefore play a potential role in the prevention of stone formation associated with hyperoxaluria.

Topics: Ammi; Animals; Calcium Oxalate; Cell Line; Cell Survival; Dogs; Epithelial Cells; Fruit; Khellin; Kidney; Kidney Calculi; L-Lactate Dehydrogenase; LLC-PK1 Cells; Oxalates; Oxalic Acid; Plant Extracts; Swine

Fruit and vegetable juices containing citrate may be recommended as an alternative in mild to moderate level hypocitraturic calcium stone formers who cannot tolerate pharmacological treatment. Tomato has been proved a citrate-rich vegetable. Tomato juice usage as citrate sources in hypocitraturic recurrent stone formers were evaluated in the light of the results of studies on orange and lemon juices. Ten 100 ml samples were prepared from three different tomato types processed through a blender. These samples were examined in terms of citrate, oxalate, calcium, magnesium, and sodium contents. No difference was detected between the parameters tested in three different tomato juices. Fresh tomato juice may be useful in hypocitraturic recurrent stone formers due to its high content of citrate and magnesium, and low content of sodium and oxalate. As the three different types of tomatoes did not differ in terms of citrate, magnesium, sodium, and oxalate content, they may be useful for clinical use if also supported by clinical studies.

Topics: Beverages; Citric Acid; Citrus; Citrus sinensis; Fruit; Kidney Calculi; Magnesium; Oxalates; Sodium; Sodium, Dietary; Solanum lycopersicum; Urolithiasis

Renal protection and antiurolithiasic effects of two extracts of Paronychia argentea (PA), a traditional Algerian plant commonly known as Algerian tea, were evaluated. This study was carried out to determine whether the aqueous extract (APA) or the butanolic extract (BPA) of aerial parts could prevent or reduce calculi aggregation in experimental calcium oxalate (Ox) nephrolithiasis in Wistar rats.. The two extracts (APA and BPA) were administrated orally and daily, during 28 days to nephrolithiasic treated rats at the dose of 250, 500 mg/kg b.w. and 10, 20mg/kg b.w. respectively. Body weight, renal index, liver index, serum level of creatinine, uric acid, urea, K(+), Ca(2+), Mg(2+), Na(+) and transaminase (alanine aminotransferase, ALT; aspartate aminotransferase, AST), phosphatase alkaline activity (PAL) were evaluated following the 28 days treatment in rats. In addition histopathological changes in kidney and liver were stained in hematoxylin eosin (HE).. The effect of the extracts could be advantageous in preventing urinary stone retention by reducing renal necrosis and thus inhibit crystal retention. In contradiction with APA, the two doses of BPA attenuated elevation in the serum creatinine (p<0.01) and blood urea levels (p<0.01) (nephroprotective effect). However, the increase in ALT (27%) and PAL (31-51%) serum levels and in the relative liver weights (p<0.01) in the groups treated with doses of APA may indicate that this extract has not a hepatoprotective effect against oxalate toxicity.. The presented data indicate that administration of the butanolic extract of aerial parts to rats with NaOx induced lithiasis, and reduced and prevented the growth of urinary stones in experimental calcium oxalate nephrolithiasis in Wistar rats.

Topics: Alanine Transaminase; Alkaline Phosphatase; Animals; Calcium Oxalate; Caryophyllaceae; Creatinine; Disease Models, Animal; Kidney; Kidney Calculi; Liver; Male; Necrosis; Nephrolithiasis; Organ Size; Oxalates; Phytotherapy; Plant Components, Aerial; Plant Extracts; Rats; Rats, Wistar; Urea

Renal stones in children, although rare, may be associated with morbidity and renal damage. Scottish children have a different ethnic composition and diet compared with paediatric populations previously studied. Urinary stone promoters include calcium, oxalate and urate. Postulated inhibitors include citrate and glycosaminoglycans (GAGs). We tested the hypothesis that Scottish paediatric stone-formers have higher excretion of urinary stone promoters (calcium/oxalate/urate) and/or lower excretion of stone inhibitors (citrate/GAGs) than children with isolated haematuria and controls.. In this case-controlled study, we measured creatinine, calcium, oxalate, urate, citrate and GAGs in random urine samples from 24 stone-formers (excluding inherited metabolic disorders), median age 10.2 (range 1.0-17.2) y; 25 patients with isolated haematuria, 6.3 (0.6-13.7) y; and 32 controls, 7.5 (0.8-14.7) y.. Excretion of urinary promoters and inhibitors differed among stone-formers, haematuria and control groups for (median (range)): calcium (0.82 (0.02-2.19), 0.43 (0.08-2.65), 0.31 (0.04-2.12) mmol/mmol creatinine, respectively, P = 0.005), citrate (0.42 (0.13-0.72), 0.33 (0.05-0.84), 0.61 (0.11-1.75) mmol/mmol creatinine, P = 0.001), calcium:citrate ratio (1.68 (0.19-4.81), 1.30 (0.19-9.57), 0.54 (0.10-2.27) mmol/mmol, P < 0.0001) and the promoter:inhibitor ratio (calcium x oxalate)/(citrate x GAGs) (8.3 (1.0-82.5), 4.3 (1.2-69.5), 2.8 (0.3-13.2) mmol/g, P < 0.0001).. Scottish paediatric stone-formers had lower urinary citrate excretion and higher urinary calcium excretion, calcium:citrate ratio and promoter:inhibitor ratio compared with controls. Urinary calcium excretion and promoter:inhibitor ratio was also higher than children with isolated haematuria. Nevertheless, marked overlap between the stone-former and haematuria groups for promoter:inhibitor and calcium:citrate ratios suggests that some patients with isolated haematuria may be at future risk of urolithiasis.

Topics: Calcium; Calcium Oxalate; Calcium, Dietary; Case-Control Studies; Child; Citrates; Creatinine; Diet; Hematuria; Hospitals, Pediatric; Humans; Kidney Calculi; Oxalates; Population Groups; Risk Factors; Scotland; Uric Acid; Urinary Calculi; Urolithiasis; White People

The epidemiological relationship between nephrolithiasis and type 2 diabetes mellitus is well-known. Patients with diabetes mellitus are at increased risk for nephrolithiasis and those with nephrolithiasis are at risk for diabetes mellitus. We examined 24-hour urine composition in stone formers with and without diabetes mellitus.. We retrospectively reviewed a database of 462 stone forming patients to examine the relationship between hypertension and 24-hour urine composition. Multivariate linear regression models were adjusted for age, race, gender, body mass index, hypertension, relevant medications and 24-hour urine constituents.. On univariate analysis diabetic patients had significantly greater urine volume than nondiabetic patients (2.5 vs 2.1 l daily, p = 0.004). Those with diabetes mellitus also excreted less daily potassium (61.1 vs 68.8 mEq, p = 0.04), phosphate (0.84 vs 1.0 gm, p = 0.002) and creatinine (1405.5 vs 1562.8 mg, p = 0.03), and had significantly lower daily urine pH (5.78 vs 6.09, p <0.001) and CaP supersaturation (0.49 vs 1.20, p <0.001) than nondiabetic patients. On multivariate analysis compared to patients without diabetes mellitus those with type II diabetes mellitus had significantly lower urine pH (-0.34, 95% CI -0.48 to -0.21) and significantly greater urine oxalate (6.43 mg daily, 95% CI 1.26 to 11.60) and volume (0.38 l daily, 95% CI 0.13 to 0.64).. Results show that of stone formers patients with type II diabetes mellitus excrete significantly greater urinary oxalate and significantly lower urine pH than those without diabetes mellitus. These findings are important for treating nephrolithiasis since they may influence dietary counseling, medical management and stone prevention.

Topics: Diabetes Mellitus, Type 2; Diabetic Nephropathies; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates; Retrospective Studies

We present here the anatomy and histopathology of kidneys from 11 patients with renal stones following small bowel resection, including 10 with Crohn's disease and 1 resection in infancy for unknown cause. They presented predominantly with calcium oxalate stones. Risks of formation included hyperoxaluria (urine oxalate excretion greater than 45 mg per day) in half of the cases, and acidic urine of reduced volume. As was found with ileostomy and obesity bypass, inner medullary collecting ducts (IMCDs) contained crystal deposits associated with cell injury, interstitial inflammation, and papillary deformity. Cortical changes included modest glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Randall's plaque (interstitial papillary apatite) was abundant, with calcium oxalate stone overgrowth similar to that seen in ileostomy, idiopathic calcium oxalate stone formers, and primary hyperparathyroidism. Abundant plaque was compatible with the low urine volume and pH. The IMCD deposits all contained apatite, with calcium oxalate present in three cases, similar to findings in patients with obesity bypass but not an ileostomy. The mechanisms for calcium oxalate stone formation in IMCDs include elevated urine and presumably tubule fluid calcium oxalate supersaturation, but a low calcium to oxalate ratio. However, the mechanisms for the presence of IMCD apatite remain unknown.

Topics: Abdomen; Adult; Apatites; Biopsy; Calcium Oxalate; Calculi; Digestive System Surgical Procedures; Female; Humans; Hyperoxaluria; Hyperparathyroidism, Primary; Ileostomy; Intestine, Small; Intestines; Kidney; Kidney Calculi; Kidney Cortex; Kidney Diseases; Male; Obesity; Oxalates; Young Adult

Much attention has been recently directed at fructose consumption because of its association with obesity and subsequent development of chronic diseases. It was recently reported that an increased fructose intake increases the risk of forming kidney stones. It was postulated that fructose consumption may increase urinary oxalate, a risk factor for calcium oxalate kidney stone disease. However, conflicting results have been obtained in human studies examining the relationship between fructose metabolism and oxalate synthesis. To test whether fructose intake influences urinary excretions impacting kidney stone risk, healthy subjects consumed diets controlled in their contents of fructose, oxalate, calcium, and other nutrients. Subjects consumed diets containing 4, 13, and 21% of calories as fructose in a randomized order. No changes in the excretions of oxalate, calcium, and uric acid were observed. In vitro investigations with cultured liver cells incubated with (13)C-labeled sugars indicated that neither fructose nor glucose was converted to oxalate by these cells. Fructose metabolism accounted for 12.4 ± 1.6% of the glycolate detected in the culture medium and glucose 6.4 ± 0.9%. Our results suggest that mechanisms for stone risk associated with fructose intake may lie in factors other than those affecting the major stone risk parameters in urine.

Topics: Adult; Calcium; Calcium Oxalate; Female; Fructose; Glycolates; Hep G2 Cells; Humans; Kidney Calculi; Male; Oxalates; Risk Factors

Primary hyperoxaluria (PH) is a rare autosomal recessive disease caused by the functional defect of alanine-glyoxylate aminotransferase (AGT) enzyme in the liver and it is characterized by the deposition of diffuse calcium oxalate crystals. A 38-year-old male patient presented with history of recurrent nephrolithiasis and has received chronic hemodialysis treatment for 2 years. Cadaveric renal transplantation was applied to the case. The patient was reoperated on postoperative day 13 because of the collection surrounding the urethra. During this operation, kidney biopsy was made due to late decrease in creatinine levels. Deposition of diffuse oxalate crystal was detected in allograft kidney biopsy, whereas in the 0-hour biopsy there were no oxalate crystals. Oxalate level was found to be high in a 24-hour urine specimen (118 mg/L, normal level: 7-44 mg/L). The patient was identified with primary hyperoxaluria and followed up in terms of systemic oxalate deposition as well as allograft kidney. In the kidney biopsy taken after 18 months, we detected that oxalate crystals almost entirely disappeared. In our case, bilateral preretinal, intraretinal, and intravascular diffuse oxalate crystals were detected, and argon laser photocoagulation treatments were needed for choroidal and retinal neovascularization. Repeated ophthalmic examinations showed the regressive nature of oxalate depositions. In the 18th month, fundus examination and fluorescein angiography revealed that oxalate crystals were significantly regressed. To increase the quality of life and slow down the systemic effects of oxalosis, kidney-only transplantation is beneficial.

Topics: Adult; Coronary Vessels; Humans; Hyperoxaluria, Primary; Kidney; Kidney Calculi; Kidney Failure, Chronic; Kidney Transplantation; Male; Oxalates; Retina; Transplantation, Homologous; Ultrasonography

Urolithiasis, the process of formation of stones in the kidneys and urinary tract, is the major clinical manifestation of hyperoxaluria. Ethylene glycol feeding resulted in hyperoxaluria with increased renal excretion of oxalate, sodium, calcium and phosphate and a decrease in the excretion of magnesium. Supplementation with an aqueous and alcoholic extract of the leaves of Salvadora persica significantly reduced elevated urinary oxalate levels, indicating a regenerative action on endogenous oxalate synthesis. The deposition of stone-forming constituents in the kidneys of calculogenic rats was also significantly lowered by curative and preventive treatments with the aqueous and alcoholic extracts of Salvadora persica. The high serum creatinine level observed in ethylene glycol-treated rats was also reduced following treatment with the extracts. Histopathological findings showed signs of improvement after treatment with the extracts. These observations led to the conclusion that the aqueous and alcoholic extracts of the leaves of Salvadora persica are endowed with antiurolithiatic properties.

Topics: Animals; Creatinine; Disease Models, Animal; Ethylene Glycol; Female; Kidney Calculi; Male; Mice; Oxalates; Plant Extracts; Plant Leaves; Rats; Rats, Wistar; Risk Factors; Salvadoraceae; Solvents; Toxicity Tests, Acute; Urolithiasis

Kidney stone analysis is the test done on the stone which cause problems when they block the flow of urine through or out of the kidneys. The stones cause severe pain and are also associated with morbidity and renal damage. There is also no clear understanding on the relative metabolic composition of renal calculi. Hence, the study is aimed to find out the chemical composition of it which can guide treatment and give information that may prevent more stones from forming. The study was carried out on the stones that had been sent to the department of Biochemistry (n = 99; M = 61; F = 38; Mean age: 33.6 +/- 14.4 years) Approximately 98.9% of stones were composed of oxalate, 95.9% of Calcium, 85.8% of phosphate, 62.6% of Urate, 46.4% of Ammonium and very few percentages of Carbonate.

Topics: Adolescent; Adult; Aged; Calcium; Carbonates; Child; Child, Preschool; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Quaternary Ammonium Compounds; Uric Acid; Young Adult

Primary hyperparathyroidism (PHPT) is often complicated by kidney stones. Hypercalciuria and urine oxalate excretion are considered risk factors for urolithiasis in PHPT as well as in idiopathic stone-formers. Recently, the anion-exchanger SLC26A6 has been involved in the oxalate metabolism.. We tested the hypothesis that the 206M polymorphic variant of SLC26A6 gene might contribute to the risk of kidney stones in PHPT. DNA samples from 145 PHPT patients and 129 age- and sex-matched healthy subjects were genotyped.. The homozygous 206V genotype was the most frequent both in PHPT patients and controls (79.3 and 74.4%), while heterozygosity for the 206M allele was detected in 20.0 and 23.3% respectively. The homozygous 206M genotype was extremely rare, occurring in 0.7 and 2.3% of PHPT and healthy subjects respectively. In the PHPT cohort, the prevalence of urolithiasis did not differ between the V/V and V/M+M/M groups and urine oxalate excretions did not correlate with the genotype. Considering the subset of PHPT stone formers (n=74), calciuria was lower in V/M+M/M patients with respect to V/V stone-formers (4.40+/-1.88 vs 5.92+/-2.62 mg/kg per 24 h; mean+/-s.d., P=0.034). Finally, the SLC26A6 206M alleles were significantly related to the presence of hypertension (73.3 vs 47.8%), showing an OR of 4.8.. Though the SLC26A6 206M polymorphism did not correlate with kidney stone development in PHPT patients, PHPT stone-formers harbouring the M allele had a lower hypercalciuria. This observation and the high prevalence of hypertension associated with the 206M polymorphism need further investigation.

Topics: Aged; Chlorides; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Hyperparathyroidism, Primary; Incidence; Italy; Kidney Calculi; Male; Membrane Transport Proteins; Middle Aged; Oxalates; Polymorphism, Genetic; Prevalence; Risk Factors; Sulfate Transporters

The pathogenesis of calcium urolithiasis involves complex interactions of urinary promoters and inhibitors of crystallization. A variety of risk formulas have been established to approximate these interactions for clinical evaluation, and the aim of our study was to determine their usefulness as predictors of stone formation. The study cohort comprised 126 patients (63 boys and 63 girls) aged 6.7-18 years (mean age 14.1 +/- 2.9 years) with calcium urolithiasis (61 with chemically confirmed calcium oxalate stones and 65 children with a strong clinical suspicion of this type of urolithiasis). Of these, 36 children were classified as recurrent stone-formers, whereas the remaining 90 had experienced only one stone episode. The values obtained were compared to those of a control group of 60 age- and gender- matched healthy children. A number of crystallization risk indices were calculated from analytes obtained in 24-h urine: calcium/magnesium ratio (Ca/Mg), calcium/citrate ratio (Ca/Cit), (calcium x oxalate)/(magnesium x citrate) ratio (CaOx/MgCit), relative urinary CaOx supersaturation (RS(CaOx)), CaOx activity product index (AP(CaOx)), and standardized CaOx activity product index (AP(CaOx stand)). All indices, except for the AP(CaOx) index, were significantly higher in stone-formers than in the controls. The Ca/Mg, Ca/Cit, CaOx/MgCit, AP(CaOx), and AP(CaOx stand) indices were significantly higher in recurrent stone-formers than in first-episode ones. However, the determination of precise cutoffs between pathological and non-pathological values was problematic due to a considerable overlap of individual values. Based on our results, we conclude that calculation of the majority of risk indices may play a rather supplementary role in the evaluation of children with calcium urolithiasis.

Topics: Adolescent; Calcium; Calcium Oxalate; Child; Citric Acid; Crystallization; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Risk Factors; Urolithiasis

The impact of the Dietary Approaches to Stop Hypertension (DASH) diet on kidney stone formation is unknown. We prospectively examined the relation between a DASH-style diet and incident kidney stones in the Health Professionals Follow-up Study (n = 45,821 men; 18 yr of follow-up), Nurses' Health Study I (n = 94,108 older women; 18 yr of follow-up), and Nurses' Health Study II (n = 101,837 younger women; 14 yr of follow-up). We constructed a DASH score based on eight components: high intake of fruits, vegetables, nuts and legumes, low-fat dairy products, and whole grains and low intake of sodium, sweetened beverages, and red and processed meats. We used Cox hazards regression to adjust for factors that included age, BMI, and fluid intake. Over a combined 50 yr of follow-up, we documented 5645 incident kidney stones. Participants with higher DASH scores had higher intakes of calcium, potassium, magnesium, oxalate, and vitamin C and had lower intakes of sodium. For participants in the highest compared with the lowest quintile of DASH score, the multivariate relative risks for kidney stones were 0.55 (95% CI, 0.46 to 0.65) for men, 0.58 (95% CI, 0.49 to 0.68) for older women, and 0.60 (95% CI, 0.52 to 0.70) for younger women. Higher DASH scores were associated with reduced risk even in participants with lower calcium intake. Exclusion of participants with hypertension did not change the results. In conclusion, consumption of a DASH-style diet is associated with a marked decrease in kidney stone risk.

Topics: Adult; Age Factors; Aged; Diet; Female; Humans; Hypertension; Kidney Calculi; Male; Middle Aged; Oxalates; Proportional Hazards Models; Prospective Studies; Risk Factors

The incidence of calcium oxalate nephrolithiasis in the US has been increasing throughout the past three decades. Biopsy studies show that both calcium oxalate nephrolithiasis and nephrocalcinosis probably occur by different mechanisms in different subsets of patients. Before more-effective medical therapies can be developed for these conditions, we must understand the mechanisms governing the transport and excretion of oxalate and the interactions of the ion in general and renal physiology. Blood oxalate derives from diet, degradation of ascorbate, and production by the liver and erythrocytes. In mammals, oxalate is a terminal metabolite that must be excreted or sequestered. The kidneys are the primary route of excretion and the site of oxalate's only known function. Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. Fecal excretion of oxalate is stimulated by hyperoxalemia in rodents, but no similar phenomenon has been observed in humans. Studies in which rats were treated with (14)C-oxalate have shown that less than 2% of a chronic oxalate load accumulates in the internal organs, plasma, and skeleton. These studies have also demonstrated that there is interindividual variability in the accumulation of oxalate, especially by the kidney. This Review summarizes the transport and function of oxalate in mammalian physiology and the ion's potential roles in nephrolithiasis and nephrocalcinosis.

Topics: Animals; Humans; Ion Transport; Kidney; Kidney Calculi; Oxalates; Risk Factors

The in vivo formation of calcium oxalate concretions having calcium phosphate nidi is simulated in an in vitro (37 degrees C, pH 6.0) dual constant composition (DCC) system undersaturated (sigma DCPD = -0.330) with respect to brushite (DCPD, CaHPO 4 . 2H 2O) and slightly supersaturated (sigma COM = 0.328) with respect to calcium oxalate monohydrate (COM, CaC2O4 . H2O). The brushite dissolution provides calcium ions that raise the COM supersaturation, which is heterogeneously nucleated either on or near the surface of the dissolving calcium phosphate crystals. The COM crystallites may then aggregate, simulating kidney stone formation. Interestingly, two intermediate phases, anhydrous dicalcium phosphate (monetite, CaHPO4) and calcium oxalate trihydrate (COT), are also detected by X-ray diffraction during this brushite-COM transformation. In support of clinical observations, the results of these studies demonstrate the participation of calcium phosphate phases in COM crystallization providing a possible physical chemical mechanism for kidney stone formation.

Topics: Calcium Phosphates; Crystallization; Kidney Calculi; Oxalates; Phosphates; Solutions; X-Ray Diffraction

Higher levels of urinary oxalate substantially increase the risk of calcium oxalate kidney stones. However, the determinants of urinary oxalate excretion are unclear. The objective was to examine the impact of dietary factors, age, body size, diabetes, and urinary factors on 24-h urinary oxalate.. We conducted a cross-sectional study of 3348 stone forming and non-stone-forming participants in the Health Professionals Follow-up Study (men), the Nurses' Health Study (older women), and the Nurses' Health Study II (younger women).. Median urinary oxalate was 39 mg/d in men, 27 mg/d in older women, and 26 mg/d in younger women. Participants in the highest quartile of dietary oxalate excreted 1.7 mg/d more urinary oxalate than participants in the lowest quartile (P trend 0.001). The relation between dietary and urinary oxalate was similar in individuals with and without nephrolithiasis. Participants consuming 1000 mg/d or more of vitamin C excreted 6.8 mg/d more urinary oxalate than participants consuming <90 mg/d (P trend < 0.001). Body mass index, total fructose intake, and 24-h urinary potassium, magnesium, and phosphorus levels also were positively associated with urinary oxalate. Calcium intake and age were inversely associated with urinary oxalate. After adjustment for body size, participants with diabetes excreted 2.0 mg/d more urinary oxalate than those without diabetes (P < 0.01).. The impact of dietary oxalate on urinary oxalate appears to be small. Further investigation of factors influencing urinary oxalate may lead to new approaches to prevent calcium kidney stones.

Topics: Adult; Age Factors; Aged; Ascorbic Acid; Body Mass Index; Body Weight; Circadian Rhythm; Cross-Sectional Studies; Diabetes Complications; Diet; Dietary Supplements; Female; Fructose; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Nutrition Assessment; Oxalates; Phosphorus; Potassium

The present study was undertaken to explore the efficiency of the pentacyclic triterpene lupeol (1) and its ester derivative, lupeol linoleate (2), in experimental hyperoxaluria. Hyperoxaluria was induced in male Wistar rats with 0.75% ethylene glycol (EG) in drinking water for 28 days. Hyperoxaluric animals were supplemented orally with 1 and 2 (50 mg/kg body wt/day) throughout the experimental period of 28 days. The renal enzymes were assayed as markers of renal tissue integrity. The redox status and oxalate metabolism in animals under oxalate overloading was also assessed. Microscopic analysis was done to investigate the abnormalities associated with oxalate exposure in renal tissues. Increase in oxidative milieu in hyperoxaluria was evident by increased lipid peroxidation (LPO) and decreased enzymic and nonenzymic antioxidants. Decrease in the activities of renal enzymes exemplified the damage induced by oxalate, which correlated positively with increased LPO and increased oxalate synthesis. Renal microscopic analysis further emphasized the oxalate-induced damage. These abnormal biochemical and histological aberrations were attenuated with test compound treatment, with 2 more effective than 1. From the present study, it can be concluded that 1 and 2 may serve as candidates for alleviating oxalate toxicity.

Topics: Administration, Oral; Animals; Disease Models, Animal; Ethylene Glycol; Hyperoxaluria; Kidney Calculi; Lipid Peroxidation; Male; Oxalates; Pentacyclic Triterpenes; Rats; Rats, Wistar; Triterpenes; Urolithiasis

The interactions between crystals and renal tubular cells are important factors in urolithiasis formation. Moreover, some reports have suggested the involvement of renal tubular cell injury in crystal-cell interaction processes. Atorvastatin, which is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, is prescribed to decrease high cholesterol levels, and it has anti-inflammation and anti-oxidization activities. Atorvastatin is also reported to control transforming growth factor-beta1 expression. We investigated whether atorvastatin can prevent renal tubular cell injury by oxalate and inhibit renal crystal retention.. Ten-week-old specific pathogen-free male Sprague-Dawley rats were used. Atorvastatin (2 mg/kg) in 0.5% carboxymethyl cellulose was administered orally daily for 2 weeks. The rats were separated into 4 experimental groups, including group 1--water and 0.5% carboxymethyl cellulose daily, group 2--water and atorvastatin in 0.5% carboxymethyl cellulose daily, group 3--1% ethylene glycol dissolved in water, 0.5 mug vitamin D3 dissolved in 1 ml salad oil and 0.5% carboxymethyl cellulose daily, and group 4--1% ethylene glycol dissolved in water, 0.5 microg vitamin D3 dissolved in 1 ml salad oil and atorvastatin in 0.5% carboxymethyl cellulose daily. The ethylene glycol model of hyperoxaluria and the effect of atorvastatin treatment were analyzed in groups 1 to 4. Urine samples were collected every 24 hours in metabolic cages and analyzed immediately or stored at -70C until analysis. The rats were sacrificed after 2 weeks and the kidneys were removed for further examination. We measured urinary N-acetyl glucosaminidase levels as a biomarker of renal tubular cell injury and urinary 8-OHdG as a biomarker of oxidative stress in 24-hour urine samples. Removed kidneys were used for quantitative analysis of the superoxide dismutase level and the detection of apoptosis. Finally, we measured the amount of crystal deposits in renal tubular cells.. Urinary N-acetyl glucosaminidase and 8-OHdG levels were decreased significantly by atorvastatin treatment in this stone forming rat model. Atorvastatin treatment increased the superoxide dismutase level and inhibited the degree of renal tubular cell N-acetyl glucosaminidase compared with stone forming control group 3. A decrease in renal crystal retention was noted when excised kidneys were evaluated following atorvastatin treatment.. Atorvastatin was found to have inhibitory effects on the renal tubular cell injury and oxidative stress caused by oxalate and crystals. Atorvastatin inhibited renal crystal retention. We believe that atorvastatin could help prevent and treat renal crystal formation.

Topics: Animals; Apoptosis; Atorvastatin; Biopsy, Needle; Disease Models, Animal; Heptanoic Acids; Immunohistochemistry; Kidney Calculi; Kidney Tubules; Male; Oxalates; Oxidative Stress; Probability; Pyrroles; Random Allocation; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; Sensitivity and Specificity; Statistics, Nonparametric; Superoxide Dismutase; Urinalysis

Fructose consumption has markedly increased over the past decades. This intake may increase the urinary excretion of calcium, oxalate, uric acid, and other factors associated with kidney stone risk. We prospectively examined the relationship between fructose intake and incident kidney stones in the Nurses' Health Study I (NHS I) (93,730 older women), the Nurses' Health Study II (NHS II) (101,824 younger women), and the Health Professionals Follow-up Study (45,984 men). Food frequency questionnaires were used to assess free fructose and sucrose intake every 4 years. Total-fructose intake was calculated as free fructose plus half the intake of sucrose, and expressed as percentage of total energy. Cox proportional hazard regressions were adjusted for age, body mass index (BMI), thiazide use, caloric intake, and other dietary factors. We documented 4902 incident kidney stones during a combined 48 years of follow-up. The multivariate relative risks of kidney stones significantly increased for participants in the highest compared to the lowest quintile of total-fructose intake for all three study groups. Free-fructose intake was also associated with increased risk. Non-fructose carbohydrates were not associated with increased risk in any cohort. Our study suggests that fructose intake is independently associated with an increased risk of incident kidney stones.

Topics: Adult; Diet; Female; Fructose; Humans; Insulin Resistance; Kidney Calculi; Magnesium; Middle Aged; Oxalates; Prospective Studies; Risk Factors

There is uncertainty about the relation between 24-h urinary uric acid excretion and the risk of calcium oxalate nephrolithiasis. In addition, the risk associated with different levels of other urinary factors needs clarification. We performed a cross-sectional study of 24-h urine excretion and the risk of kidney stone formation in 3350 men and women, of whom 2237 had a history of nephrolithiasis. After adjusting for other urinary factors, urinary uric acid had a significant inverse association with stone formation in men, a marginal inverse association with risk in younger women, and no association in older women. The risk of stone formation in men and women significantly rose with increasing urine calcium and oxalate, and significantly decreased with increasing citrate and urine volume, with the change in risk beginning below the traditional normal thresholds. Other urinary factors were also associated with risk, but this varied by age and gender. Our study does not support the prevailing belief that higher urine uric acid excretion increases the risk for calcium oxalate stone formation. In addition, the current definitions of normal levels for urinary factors need to be re-evaluated.

Topics: Adult; Aged; Calcium; Citric Acid; Cross-Sectional Studies; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Risk; Uric Acid

Nephrolithiasis and renal failure secondary to severe hyperoxaluria were complications of jejunoileal bypass for obesity, leading to the discontinuation of this procedure in the United States in 1980. Bariatric procedures currently in use have not been adequately evaluated for this complication.. We compared 24-hour urine chemistry studies of 132 patients with nephrolithiasis who had undergone bariatric surgery with the urine chemistry studies of patients who had undergone jejunoileal bypass, those with routine kidney stones and normal subjects. The primary aim was to determine if hyperoxaluria developed in patients who underwent bariatric surgery and had kidney stones as had been seen with jejunoileal bypass.. Patients who have undergone modern bariatric surgery had an adjusted mean urine oxalate excretion of 83 mg per day compared to 39 mg per day for routine kidney stone formers and 34 mg per day for normal subjects (p <0.001 for both comparisons), but not quite as high as that found in patients treated with jejunoileal bypass (102 mg per day, p <0.001). Urine supersaturation of calcium oxalate, the main driving force for calcium oxalate stone formation, was higher in patients treated with bariatric surgery compared to routine kidney stone formers and normal subjects (p <0.001 for both comparisons).. Hyperoxaluria is the most significant abnormality of urine chemistry studies in patients with kidney stones who have undergone bariatric surgery. Many of these patients have a degree of hyperoxaluria that could lead to kidney failure. Further studies are required to determine the prevalence of this problem in patients who have undergone bariatric surgery.

Topics: Bariatric Surgery; Female; Humans; Hyperoxaluria; Jejunoileal Bypass; Kidney Calculi; Male; Multivariate Analysis; Obesity; Oxalates

Topics: Colonoscopy; Crohn Disease; Diagnosis, Differential; Humans; Kidney Calculi; Kidney Failure, Chronic; Male; Middle Aged; Oxalates; Risk Factors; Tomography, X-Ray Computed

In order to compare the effects of several experimental renal calcium oxalate stones formation models in rats and to find a simple and convenient model with significant effect of calcium oxalate crystals deposition in the kidney, several rat models of renal calcium oxalate stones formation were induced by some crystal-inducing drugs (CID) including ethylene glycol (EG), ammonium chloride (AC), vitamin D(3)[1alpha(OH)VitD(3), alfacalcidol], calcium gluconate, ammonium oxalate, gentamicin sulfate, L-hydroxyproline. The rats were fed with drugs given singly or unitedly. At the end of experiment, 24-h urines were collected and the serum creatinine (Cr), blood urea nitrogen (BUN), the extents of calcium oxalate crystal deposition in the renal tissue, urinary calcium and oxalate excretion were measured. The serum Cr levels in the stone-forming groups were significantly higher than those in the control group except for the group EG+L-hydroxyproline, group calcium gluconate and group oxalate. Blood BUN concentration was significantly higher in rats fed with CID than that in control group except for group EG+L-hydroxyproline and group ammonium oxalate plus calcium gluconate. In the group of rats administered with EG plus Vitamin D(3), the deposition of calcium oxalate crystal in the renal tissue and urinary calcium excretion were significantly greater than other model groups. The effect of the model induced by EG plus AC was similar to that in the group induced by EG plus Vitamin D(3). EG plus Vitamin D(3) or EG plus AC could stably and significantly induced the rat model of renal calcium oxalate stones formation.

Topics: Ammonium Chloride; Animals; Blood Urea Nitrogen; Calcium; Calcium Gluconate; Calcium Oxalate; Creatinine; Crystallization; Disease Models, Animal; Ethylene Glycol; Gentamicins; Hydroxycholecalciferols; Hydroxyproline; Kidney; Kidney Calculi; Magnesium; Male; Microscopy, Polarization; Oxalates; Phosphorus; Random Allocation; Rats; Rats, Wistar

This work focuses on the behavior of in vitro calcium oxalate crystallization. The effects of several compounds on the kinetics of calcium oxalate crystallization were examined.. Rates of nucleation and aggregation of calcium oxalate crystals were derived from 30-min time-course measurements of optic density at 620 nm after mixing solutions containing calcium chloride and sodium oxalate at 37 degrees C, pH 5.7. The maximum increase of optic density with time, termed S(N), mainly reflects maximum rate of formation of new particles and thus crystal nucleation. After equilibrium has been reached, optic density decreases. No new particles were formed due to crystal aggregation. S(A) (the maximum slope of decrease of optic density at 620 nm with time, representing crystal aggregation) is derived from the maximum decrease in optic density.. Among the modifiers studied, citrate decreased both S(N) and S(A) (P < 0.001). Magnesium was also found to inhibit the rate of nucleation and crystal aggregation, but it appeared in a non-concentrated manner. Nucleation and aggregation inhibition ratios were related inversely to concentration of albumin (P < 0.001).. The growth and agglomeration of calcium oxalate crystals are differently modulated by various compounds. The treatments aiming at inhibiting crystallization of calcium oxalate can be better defined by these findings. And new treatment modalities can be developed.

Topics: Anticoagulants; Calcium; Calcium Oxalate; Citrates; Crystallization; Humans; In Vitro Techniques; Kidney Calculi; Oxalates; Spectrophotometry

Grain amaranth (Amaranthus spp.) is a widely adaptable C4 pseudo-cereal crop that has interesting nutritional characteristics including high protein and calcium concentrations and a lack of gluten. To date, no antinutrient has been found at problematic levels in grain amaranth; however, oxalate has not been thoroughly studied. Dietary oxalate is a potential risk factor for kidney stone development, and its presence in food lowers calcium and magnesium availability. Oxalate concentration and forms and calcium and magnesium concentrations were determined in 30 field-grown grain amaranth genotypes from the species A. cruentus, A. hybrid, and A. hypochondriacus. The effects of seeding date and fertilization with calcium ammonium nitrate were evaluated in field experiments conducted in multiple environments; the effects of cooking were also evaluated. Mean total oxalate concentration in the 30 genotypes analyzed was 229 mg/100 g, with values ranging between 178 and 278 mg/100 g, the greatest proportion being insoluble (average of 80%). Calcium concentration averaged 186 mg/100 g and ranged between 134 and 370 mg/100 g, whereas magnesium averaged 280 mg/100 g and ranged between 230 and 387 mg/100 g. Fertilization only marginally increased total oxalate concentration and had no effects on other variables. Seeding date had no effects on any of the variables studied. Boiling increased the proportion of soluble oxalate but did not affect total oxalate concentration. Grain amaranth can be considered a high oxalate source, however, as most is in insoluble form, and due to its high calcium and magnesium concentrations, oxalate absorbability could be low. This should be confirmed by bioavailability studies.

Topics: Amaranthus; Calcium; Cooking; Diet; Edible Grain; Humans; Kidney Calculi; Magnesium; Oxalates; Reproduction; Risk Factors

The goal of this work is to analyze clinical and therapeutics particularities of primary hyperoxaluria in children in Tunisian centre.. We studied retrospectively 15 cases of primary hyperoxaluria enrolled during 9 years period (1994-2002).. It is about 2 boys and 13 girls (sex - ratio = 4.5) aged 2 month to 13 years (mean age: 4 years). Six patients presented the infantile form and nine the juvenile form of HP. At the moment of diagnosis, renal function was normal in one patient, moderately altered in another and severely altered in the other patients. All patients had nephrocalcinosis and 6 among them radio-opaque renal calculi associated. Diagnosis of HP was established in 11 cases by hyperoxaluria and/or important hyperoxalemia or on the data of the renal biopsy and biochemical analysis of renal calculi in 4 cases. The so-called "maghrebin" mutation (Ile244Thr) sought-after in 9 children, has cannot be identified that in 2 among them. Eight patients died of the continuations of their illness. The seven other patients again in life present a terminal renal insufficiency treated by haemodialysis. No patient could benefit from organ transplantation.. Primary hyperoxaluria is a very heterogeneous disease on the plan clinic that genetic. In Tunisia where it constitutes a frequent cause of end stage renal failure, prenatal diagnosis of this disease is of a big interest.

Topics: Adolescent; Biopsy; Child; Child, Preschool; Female; Humans; Hyperoxaluria, Primary; Infant; Isoleucine; Kidney; Kidney Calculi; Kidney Failure, Chronic; Male; Mutation; Nephrocalcinosis; Oxalates; Retrospective Studies; Survival Rate; Threonine; Tunisia

Nephrocalcinosis is the result of a myriad of hereditary or acquired diseases in the calcium, phosphate or oxalate metabolism that lead to deposition of calcium containing precipitates within the kidney. Nephrocalcinosis and nephrolithiasis are pathophysiologically tightly related and often co-exist. In the case of recurrent nephrolithiasis, nephrocalcinosis has to be excluded. Stone analysis can yield important clues to the underlying disease process. The best way to diagnose nephrocalcinosis and an accompanying nephrolithiasis is by native computer tomography scans. Untreated, nephrocalcinosis will lead to a progressive decline in renal function and eventually to end stage renal disease. Thus, for each case, the underlying disease process has to be determined and a causative therapy initiated.

Topics: Calcium; Diagnosis, Differential; Humans; Hyperparathyroidism, Primary; Kidney; Kidney Calculi; Kidney Function Tests; Nephrocalcinosis; Oxalates; Parathyroid Hormone; Phosphates; Tomography, X-Ray Computed

The intestinal organism Oxalobacter formigenes is unique in using oxalate as its primary carbon and energy source. Intestinal colonization with O. formigenes may have clinical significance by decreasing intestinal oxalate and its absorption, thereby influencing the concentration of oxalate in plasma and urine, and the development of calcium oxalate stone disease. Because the oxalate content of the diet varies considerably, we hypothesized that the number of O. formigenes and amount of oxalate would vary in feces.. To enumerate the number of O. formigenes in feces an accurate and reproducible real-time polymerase chain reaction assay was developed to quantify O. formigenes DNA. Stool samples were obtained from 10 colonized individuals to determine the levels of O. formigenes by this assay and the oxalate content by ion chromatography.. Concentrations of O. formigenes ranged from lower than the limit of detection of 5 x 10(3) to 1.04 x 10(9) cells per gm stool. The total oxalate content of stool samples varied from 0.1 to 1.8 mg/gm and fecal water oxalate varied from 60 to 600 microM. All parameters measured varied within each stool collection, among stool collections on different days and among individuals. Notably in 7 of 10 individuals at least 1 stool sample contained no detectable O. formigenes. In addition, 7 of 10 subjects had a fecal colonization of less than 4 x 10(4) per gm stool.. This study demonstrates that there is intrastool and interstool sample variability in the amount of O. formigenes measured by real-time polymerase chain reaction that did not correlate with the quantity of oxalate in stool. Most subjects had a fecal colonization of less than 4 x 10(4) per gm stool.

Topics: Adult; Chromatography, Ion Exchange; Colony Count, Microbial; DNA, Bacterial; Feces; Female; Flow Cytometry; Humans; Intestinal Absorption; Intestinal Mucosa; Intestines; Kidney Calculi; Male; Oxalates; Oxalobacter formigenes; Polymerase Chain Reaction; Reproducibility of Results

The assumption of oxidative stress as a mechanism in oxalate induced renal damage suggests that antioxidants might play a beneficial role against oxalate toxicity. An in vivo model was used to investigate the effect of C-phycocyanin (from aquatic micro algae; Spirulina spp.), a known antioxidant, against calcium oxalate urolithiasis. Hyperoxaluria was induced in two of the 4 groups of Wistar albino rats (n = 6 in each) by intraperitoneally injecting sodium oxalate (70 mg/kg body weight). A pretreatment of phycocyanin (100 mg/kg body weight) as a single oral dosage was given, one hour prior to oxalate challenge. An untreated control and drug control (phycocyanin alone) were employed. Phycocyanin administration resulted in a significant improvement (p < 0.001) in the thiol content of renal tissue and RBC lysate via increasing glutathione and reducing malondialdehyde levels in the plasma of oxalate induced rats (p < 0.001), indicating phycocyanin's antioxidant effect on oxalate mediated oxidative stress. Administering phycocyanin after oxalate treatment significantly increased catalase and glucose-6-phosphate dehydrogenase activity (p < 0.001) in RBC lysate suggesting phycocyanin as a free radical quencher. Assessing calcium oxalate crystal retention in renal tissue using polarization microscopy and renal ultrastructure by electron microscopy reveals normal features in phycocyanin-- pretreated groups. Thus the study presents positive pharmacological implications of phycocyanin against oxalate mediated nephronal impairment and warrants further work to tap this potential aquatic resource for its medicinal application.

Topics: Animals; Antioxidants; Calcium Oxalate; Erythrocytes; Glutathione; Kidney; Kidney Calculi; Lipid Peroxidation; Male; Malondialdehyde; Microscopy, Electron; Microscopy, Polarization; Nephrons; Oxalates; Oxidative Stress; Phycocyanin; Rats; Rats, Wistar

Topics: Animals; Antiporters; Gastrointestinal Tract; Homeostasis; Kidney Calculi; Mice; Mice, Knockout; Oxalates; Sulfate Transporters

Detailed knowledge of food oxalate content is of essential importance for dietary treatment of recurrent calcium oxalate urolithiasis. Dietary oxalate can contribute considerably to the amount of urinary oxalate excretion. Because cereal foods play an important role in daily nutrition, the soluble and total oxalate contents of various types of cereal grains, milling products, bread, pastries, and pasta were analyzed using an HPLC-enzyme-reactor method. A high total oxalate content (>50 mg/100 g) was found in whole grain wheat species Triticum durum (76.6 mg/100 g), Triticum sativum (71.2 mg/100 g), and Triticum aestivum (53.3 mg/100 g). Total oxalate content was comparably high in whole grain products of T. aestivum, that is, wheat flakes and flour, as well as in whole grain products of T. durum, that is, couscous, bulgur, and pasta. The highest oxalate content was demonstrated for wheat bran (457.4 mg/100 g). The higher oxalate content in whole grain than in refined grain cereals suggests that oxalic acid is primarily located in the outer layers of cereal grains. Cereals and cereal products contribute to the daily oxalate intake to a considerable extent. Vegetarian diets may contain high amounts of oxalate when whole grain wheat and wheat products are ingested. Recommendations for prevention of recurrence of calcium oxalate stone disease have to take into account the oxalate content of these foodstuffs.

Topics: Bread; Calcium Oxalate; Edible Grain; Flour; Food Handling; Humans; Kidney Calculi; Oxalates; Solubility; Triticum

The Zellweger spectrum disorders (ZSDs) are characterized by a generalized loss of peroxisomal functions caused by deficient peroxisomal assembly. Clinical presentation and survival are heterogeneous. Although most peroxisomal enzymes are unstable in the cytosol of peroxisome-deficient cells of ZSD patients, a few enzymes remain stable among which alanine:glyoxylate aminotransferase (AGT). Its deficiency causes primary hyperoxaluria type 1 (PH1, MIM 259900), an inborn error of glyoxylate metabolism characterized by hyperoxaluria, nephrocalcinosis, and renal insufficiency. Despite the normal level of AGT activity in ZSD patients, hyperoxaluria has been reported in several ZSD patients. We observed the unexpected occurrence of renal stones in a cohort of ZSD patients. This led us to perform a study in this cohort to determine the prevalence of hyperoxaluria in ZSDs and to find clinically relevant clues that correlate with the urinary oxalate load. We reviewed medical charts of 31 Dutch ZSD patients with prolonged survival (>1 year). Urinary oxalate excretion was assessed in 23 and glycolate in 22 patients. Hyperoxaluria was present in 19 (83%), and hyperglycolic aciduria in 14 (64%). Pyridoxine treatment in six patients did not reduce the oxalate excretion as in some PH1 patients. Renal involvement with urolithiasis and nephrocalcinosis was present in five of which one developed end-stage renal disease. The presence of hyperoxaluria, potentially leading to severe renal involvement, was statistically significant correlated with the severity of neurological dysfunction. ZSD patients should be screened by urinalysis for hyperoxaluria and renal ultrasound for nephrocalcinosis in order to take timely measures to prevent renal insufficiency.

Topics: Adolescent; Child; Child, Preschool; Cohort Studies; Glycolates; Humans; Hyperoxaluria; Infant; Kidney Calculi; Oxalates; Renal Insufficiency; Retrospective Studies; Zellweger Syndrome

Hyperoxaluria is a risk factor for renal stones. It appears to be sustained by increased dietary load or increased intestinal absorption. The aim of this study was to evaluate whether oral administration of lactobacilli could prevent urolithiasis in stone-forming rats. Oxalate-degrading activities of lactobacilli were evaluated by measuring the oxalate level in a culture medium after inoculation with lactobacilli. Only the strains of Lactobacillus having oxalate-degrading activity were used. Sprague-Dawley rats were fed a powdered standard diet containing 3% sodium oxalate and/or received 100 mg/kg of celecoxib for the first 8 days by gavage, before or after the beginning of this experiment (groups with previous treatment or with co-treatment). Rats were sacrificed after 4 weeks and kidneys were harvested for the assay of crystal formation under a dissecting microscope. Twenty-four-hour urine collections were performed before kidney harvest. Only two strains, Lactobacillus casei HY2743 and L. casei HY7201 out of 31 strains of Lactobacillus were able to degrade oxalate. In both groups of co-treatment and previous treatment with L. casei HY2743 and L. casei HY7201, urine oxalate excretion decreased compared to the group without lactobacilli. The dissecting microscope examination of kidneys in the rats in two previous treatment groups and the co-treatment group with L. casei HY7201 showed less abundant crystals than control groups. Our results show that lactobacilli may be used as a potential therapeutic strategy in the prevention of urinary stones.

Topics: Animals; Body Weight; Citric Acid; Crystallization; Kidney; Kidney Calculi; Lactobacillus; Male; Oxalates; Pilot Projects; Rats; Rats, Sprague-Dawley

Calcium oxalate monohydrate (COM) crystals are the commonest component of kidney stones. Oxalate and COM crystals in renal cells are thought to contribute to pathology via prooxidant events. Using an in vivo rat model of crystalluria induced by hyperoxaluria plus hypercalciuria [ethylene glycol (EG) plus 1,25-dihydroxycholecalciferol (DHC)], we measured glutathione and energy homeostasis of kidney mitochondria. Hyperoxaluria or hypercalciuria without crystalluria was also investigated. After 1-3 wk of treatment, kidney cryosections were analyzed by light microscopy. In kidney subcellular fractions, glutathione and antioxidant enzymes were measured. In mitochondria, oxygen consumption and superoxide formation as well as cytochrome c content were measured. EG plus DHC treatment increased formation of renal birefringent crystal. Histology revealed increased renal tubular pathology characterized by obstruction, distension, and interstitial inflammation. Crystalluria at all time points led to oxidative stress manifest as decreased cytosolic and mitochondrial glutathione and increased activity of the antioxidant enzymes glutathione reductase and -peroxidase (mitochondria) and glucose-6-phosphate dehydrogenase (cytosol). These changes were followed by a significant decrease in mitochondrial cytochrome c content at 2-3 wk, suggesting the involvement of apoptosis in the renal pathology. Mitochondrial oxygen consumption was severely impaired in the crystalluria group without increased mitochondrial superoxide formation. Some of these changes were also evident in hyperoxaluria at week 1 but were absent at later times and in all calciuric groups. Our data indicate that impaired electron flow did not cause superoxide formation; however, mitochondrial dysfunction contributes to pathological events when tubular crystal-cell interactions are uncontrolled, as in kidney stones disease.

Topics: Animals; Calcium; Calcium Oxalate; Cytochromes c; Cytosol; Disease Models, Animal; Energy Metabolism; Glutathione; Kidney; Kidney Calculi; Male; Mitochondria; Oxalates; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Reference Values

We evaluated whether epigallocatechin gallate (EGCG), a main constituent of green tea polyphenols, could protect against cellular toxicity by oxalate and whether green tea supplementation attenuates the development of nephrolithiasis in an animal model.. Cells of the NRK-52E line were incubated with different concentrations of oxalate with and without EGCG, and toxicity and malondialdehyde assays were done to investigate the cytotoxic effect of oxalate and the anti-oxalate effect of EGCG.. In a second series of experiments, male Sprague-Dawley rats were divided into three groups. Group 1 animals (controls) were fed regular chow and drank water ad libitum; group 2 animals were fed chow containing 3% sodium oxalate with the administration of gentamicin (40 mg/kg) and drank water ad libitum; group 3 animals were fed the same diet as group 2 with gentamicin administration and drank only green tea. Rats were killed 4 weeks later after a 24-hour urine collection, and the kidneys were removed for morphologic examination.. As oxalate concentrations increased, the number of surviving cells decreased, and the formation of free radicals increased. The administration of EGCG inhibited free-radical production induced by oxalate. Green tea supplementation decreased the excretion of urinary oxalate and the activities of urinary gammaglutamyltranspeptidase and N-acetylglucosaminidase. The number of crystals within kidneys in group 3 was significantly lower than in group 2.. Green tea has an inhibitory effect on urinary stone formation, and the antioxidative action of EGCG is considered to be involved.

Topics: Acetylglucosaminidase; Animals; Antioxidants; Catechin; Cell Line; Cell Survival; Cells, Cultured; Epithelium; Free Radicals; gamma-Glutamyltransferase; In Vitro Techniques; Kidney Calculi; Kidney Tubules, Proximal; Lipid Peroxidation; Male; Malondialdehyde; Oxalates; Rats; Rats, Sprague-Dawley; Tea

To test whether increasing dietary calcium intake prevents calcium oxalate stone formation when the diet is oxalate-rich. Material and methods. Four groups, eight rats in each, were subjected to a lithogenic diet by the addition of 0.5% ethylene glycol to drinking water for 3 weeks. The first group, used as a control, simultaneously received a standard diet. The second group was supplemented with calcium at 500 mg/100 g of diet and the third group with oxalate at 3 g/100 g of diet. The diet given to the last group was supplemented with similar doses of calcium and oxalate. One day before the end of treatment, each animal was placed in a metabolic cage to collect 24-h urine samples and determine urinary parameters. The kidneys were removed to determine calcium oxalate deposits and for histological examination.. The number of calcium oxalate crystals in renal tissue was highest in the oxalate group and calcium oxalate deposits were also found to be elevated in this group. Hyperoxaluria and hypocitraturia, induced by a oxalate-rich diet, seemed to be the major causes contributing to aggravated renal stone formation. The protective effect of dietary calcium supplementation, which was clear in the calcium + oxalate group, was probably due to intestinal binding of oxalate by calcium, thereby reducing urinary oxalate excretion.. Increased dietary calcium intake can prevent calcium oxalate stone formation only when the diet is oxalate-rich.

Topics: Animals; Calcium Oxalate; Calcium, Dietary; Crystallization; Diet; Kidney; Kidney Calculi; Oxalates; Rats

A number of animal models have been developed to investigate calcium oxalate (CaOx) nephrolithiasis. Ethylene glycol (EG)-induced hyperoxaluria in rats is most common, but is criticized because EG and some of its metabolites are nephrotoxic and EG causes metabolic acidosis. Both oxalate (Ox) and CaOx crystals are also injurious to renal epithelial cells. Thus, it is difficult to distinguish the effects of EG and its metabolites from those induced by Ox and CaOx crystals. This study was performed to investigate hydroxy-L-proline (HLP), a common ingredient of many diets, as a hyperoxaluria-inducing agent. In rats, HLP has been shown to induce CaOx nephrolithiasis in only hypercalciuric conditions. Five percent HLP mixed with chow was given to male Sprague-Dawley rats for 63 days, resulting in hyperoxaluria, CaOx crystalluria, and nephrolithiasis. Crystal deposits were surrounded by ED-1-positive inflammatory cells. Cell injury and death was followed by regeneration, as suggested by an increase in proliferating cell nuclear antigen-positive cells. Both osteopontin (OPN) and CD44 were upregulated. Staining for CD44 and OPN was intense in cells lining the tubules that contained crystals. Along with a rise in urinary Ox and lactate dehydrogenase, there were significant increases in 8-isoprostane and hydrogen peroxide excretion, indicating that the oxidative stress induced cell injury. Thus, HLP-induced hyperoxaluria alone can induce CaOx nephrolithiasis in rats.

Topics: Animals; Calcium; Calcium Oxalate; Creatinine; Dinoprost; Disease Models, Animal; Gene Expression Regulation; Hyaluronan Receptors; Hydrogen Peroxide; Hydroxyproline; Hyperoxaluria; Immunohistochemistry; Kidney Calculi; Kidney Tubules; L-Lactate Dehydrogenase; Male; Osteopontin; Oxalates; Rats; Rats, Sprague-Dawley; Sialoglycoproteins

Metabolic evaluation of stone-forming (SF) patients is based on the determination of calcium, oxalate, citrate, uric acid and other parameters in 24-h urine samples under a random diet. A reliable measurement of urinary oxalate requires the collection of urine in a receptacle containing acid preservative. However, urinary uric acid cannot be determined in the same sample under this condition. Therefore, we tested the hypothesis that the addition of preservatives (acid or alkali) after urine collection would not modify the results of those lithogenic parameters. Thirty-four healthy subjects (HS) were submitted to two non-consecutive collections of 24-h urine. The first sample was collected in a receptacle containing hydrochloric acid (HCl 6 N) and the second in a dry plastic container, with HCl being added as soon as the urine sample was received at the laboratory. Additionally, 34 HS and 34 SF patients collected a spot urine sample that was divided into four aliquots, one containing HCl, another containing sodium bicarbonate (NaHCO(3 )5 g/l), and two others in which these two preservative agents were added 24 h later. Urinary oxalate, calcium, magnesium, citrate, creatinine and uric acid were determined. Urinary parameters were also evaluated in the presence of calcium oxalate or uric acid crystals. Mean values of all urinary parameters obtained from previously acidified 24-h urine samples did not differ from those where acid was added after urine collection. The same was true for spot urine samples, with the exception of urinary citrate that presented a slight albeit significant change of 5.9% between samples in HS and 3.1% in SF. Uric acid was also not different between pre- and post-alkalinized spot urine samples. The presence of crystals did not alter these results. We concluded that post-delivery acidification or alkalinization of urine samples does not modify the measured levels of urinary oxalate, calcium, magnesium, creatinine and uric acid, and that the change on citrate was not relevant, hence allowing all parameters to be determined in a single urine sample, thus avoiding the inconvenience and cost of multiple 24-h urine sample collections.

Topics: Acids; Adult; Alkalies; Calcium; Chemistry, Clinical; Citric Acid; Creatinine; Crystallization; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Preservation, Biological

The paper comparatively analyzes the effect of the mineral water "Penta" on the biochemical parameters of blood and urine, which characterize the functional activity of renal metabolic processes. A group comprising 10 examinees without renal disease took water by the routine mineral water scheme for 4 days. Comparison of the biochemical parameters before and after water taking revealed a significant reduction in azotemia and uric acid levels with its simultaneously enhanced excretion, as well as an increasing tendency for the excretion of oxalates, i.e. the most important parameters determining the formation of urate and oxalate calculi. These findings allow use "Penta", to a certain degree, in the treatment of renal disease, urolithiasis in particular, and in the prevention of stone formation.

Topics: Azotemia; Female; Humans; Kidney Calculi; Male; Mineral Waters; Oxalates; Time Factors; Uric Acid

In herbal treatment of kidney stones, antilithics are used to "dissolve" the stones or aid their passing to guard against further retention. Diuretic action is also needed to increase the amount of fluid going through the kidneys and flush out the deposits. Previous clinical studies have shown that herbal medicines and their concoctions could be used to inhibit calcium oxalate crystallization. However, the pharmacodynamics and in-vitro effects of such medicines have not been established. Five Chinese herbal medicines were selected based on their usefulness in treating stone disease. A 96-well plate oxalate-induced turbidity in artificial urine was used to evaluate the efficacies of the different herbal medicines on calcium oxalate crystallization. The metastable limit was determined and the nucleation rate was derived from 12-min time-course measurement of turbidity at 405 nm. Phase-contrast microscopy was used to visualize the crystals. The results showed that with increasing concentrations of herbal extracts, smaller calcium oxalate crystal sizes were observed. Overall, the five herbal medicinal extracts tested were able to promote nucleation of calcium oxalate crystals while at the same time decreasing the size. This in-vitro crystallization confirms that prophylaxis of renal stones could be achieved by reducing overall supersaturation through promotion of small crystal nucleates and concomitant pharmacological diuretic action of herbal medicines. Clinical studies will provide more definitive conclusions.

Topics: Calcium Oxalate; Crystallization; Drugs, Chinese Herbal; Kidney Calculi; Microscopy, Phase-Contrast; Oxalates

Greater body mass index (BMI) is a risk factor for kidney stones. However, the relation between BMI and the urinary excretion of many lithogenic factors remains unclear.. We studied urine pH, urine volume, and 24-hour urinary excretion of calcium, oxalate, citrate, uric acid, sodium, magnesium, potassium, phosphate, and creatinine in stone-forming and non-stone-forming participants in the Health Professionals Follow-Up Study (599 stone-forming and 404 non-stone-forming men), Nurses' Health Study (888 stone-forming and 398 non-stone-forming older women), and Nurses' Health Study II (689 stone-forming and 295 non-stone-forming younger women). Each cohort was divided into quintiles of BMI. Tests of linear trend were conducted by 1-way analysis of variance. Linear regression models were adjusted for age, history of stone disease, dietary intake, and urinary factors.. Participants with greater BMIs excreted more urinary oxalate (P for trend

Topics: Adult; Body Mass Index; Calcium; Calcium Oxalate; Citrates; Comorbidity; Creatinine; Diabetes Mellitus; Female; Humans; Hydrogen-Ion Concentration; Hypertension; Kidney Calculi; Linear Models; Magnesium; Middle Aged; Obesity; Oxalates; Phosphates; Potassium; Risk Factors; Sodium; Urine

Ethylene glycol (EG) consumption is commonly employed as an experimental regimen to induce hyperoxaluria in animal models of calcium oxalate nephrolithiasis. This approach has, however, been criticized because EG overdose induces metabolic acidosis in humans. We tested the hypothesis that EG consumption (0.75% in drinking water for 4 wk) induces metabolic acidosis by comparing arterial blood gases, serum electrolytes, and urinary chemistries in five groups of Sprague-Dawley rats: normal controls (CON), those made hyperoxaluric (HYP) with EG administration, unilaterally nephrectomized controls (UNI), unilaterally nephrectomized rats fed EG (HRF), and a metabolic acidosis (MA) reference group imbibing sweetened drinking water (5% sucrose) containing 0.28 M NH4Cl. Arterial pH, plasma bicarbonate concentrations, anion gap, urinary pH, and the excretion of titratable acid, ammonium, phosphate, citrate, and calcium in HYP rats were not significantly different from CON rats, indicating that metabolic acidosis did not develop in HYP rats with two kidneys. Unilateral nephrectomy alone (UNI group) did not significantly affect arterial pH, plasma bicarbonate, anion gap, or urinary pH compared with CON rats; however, HRF rats exhibited some signs of a nascent acidosis in having an elevated anion gap, higher phosphate excretion, lower urinary pH, and an increase in titratable acid. Frank metabolic acidosis was observed in the MA rats: decreased arterial pH and plasma HCO3(-) concentration with lower urinary pH and citrate excretion with elevated excretion of ammonium, phosphate and, hence, titratable acid. We conclude that metabolic acidosis does not develop in conventional EG treatments but may ensue with renal insufficiency resulting from an oxalate load.

Topics: Acidosis; Animals; Carbon Dioxide; Disease Models, Animal; Electrolytes; Ethylene Glycol; Hyperoxaluria; Kidney Calculi; Kidney Failure, Chronic; Kidney Function Tests; Male; Oxalates; Oxygen; Rats; Rats, Sprague-Dawley

It has been shown that a strong hyperbolic relationship exists between the urinary concentration of free Ca ions ([Ca]) and the amount of ammonium oxalate (Ox) that must be titrated in a standardized procedure to a urine sample to induce CaOx crystallization. The ratio of [Ca] to (Ox) is termed the Bonn Risk Index (BRI). Most data plot around a hyperbola described by the formula, [Ca] x (Ox) = constant. Due to the high relationship between [Ca] and (Ox) one may argue that determining only 1 of the 2 BRI parameters, preferably [Ca], is sufficient to describe the urine crystallization risk.. Based on 195 urine samples taken from CaOx stone formers and healthy subjects we compared the sensitivity and specificity of BRI, and its corresponding [Ca] value by calculating ROC curves. Furthermore, ROC curves of the established risk indexes, namely the model value of urinary supersaturation and the model value of the urine activity product, are presented.. Our results clearly demonstrate that 1) BRI has the highest sensitivity and specificity of the tested indexes, 2) (Ox) cannot be reliably predicted from [Ca] and 3) determining [Ca] alone revealed a meaningful first estimate of urine CaOx crystallization risk according to BRI.. To avail ourselves of the high quality of BRI in patient treatment the additional determination of (Ox) is required.

Topics: Calcium; Calcium Oxalate; Humans; Kidney Calculi; Oxalates; Reference Values; Risk; ROC Curve; Sensitivity and Specificity

Nephrolithiasis is the most important clinical manifestation of primary hyperparathyroidism (PHPT), although nowadays this disorder is often asymptomatic. Clinical or biochemical differences between PHPT patients with and without nephrolithiasis have not been clearly identified in most of the previous studies. The aim of the study was to investigate clinical and biochemical parameters in kidney stone former (SF) and non-stone former (NSF) patients with PHPT in order to identify potential risk factors. Serum and plasma samples from 55 consecutive patients (43 females, 12 males) with PHPT were collected after overnight fasting; 24-h urine collection and a fresh sample of urine for sediment analysis were obtained from all patients. Clinical data were recorded in all. Out of 55 patients, 22 had kidney stones, which were symptomatic in 73%. SFs showed circulating PTH, total and ionized calcium, 1,25 dihydroxyvitamin D3, urinary calcium excretion and 24-h urine oxalate levels significantly higher than NSFs. Hypercalciuria was often concomitant with massive quantities of calcium oxalate crystals in urine sediment. Hypercalciuria and relatively high oxaluria were associated with stone formation with an odds ratio (OR) of 4.0 and 7.0, respectively, which rose to 33.5 when they coexisted. Hypomagnesuria and hypocitraturia were common in at least one third of all PHPT patients, but they were not associated to an increased OR. As expected, they were positively correlated with urine calcium excretion, suggesting that calcium, magnesium and citrate are commonly regulated at renal level. In conclusion, hypercalciuria, higher oxalate excretion and severe PHPT are associated with kidney stones in PHPT.

Topics: Aged; Calcium; Calcium Oxalate; Cholecalciferol; Female; Humans; Hyperparathyroidism; Kidney; Kidney Calculi; Male; Middle Aged; Oxalates; Risk Factors; Severity of Illness Index

Anemia is an important cause of morbidity in patients suffering from chronic renal failure, and erythropoietin is a milestone of anemia treatment. Various factors may cause erythropoietin resistance. Herein, we describe the case of 32-year-old man who presented with anemia and weakness. He developed progressive renal failure secondary to recurrent kidney stones. One year before admission, he developed anemia for which he had been treated with erythropoietin. However, the anemia persisted. Examination of bone marrow biopsy specimen showed that the marrow was extensively replaced with oxalate crystals and fibrous connective tissue with severe decrease of hematopoietic cells. To the best of our knowledge, our patient represents the first case in the literature describing the association between the oxalate deposition and EPO resistance.

Topics: Adult; Anemia; Biopsy, Needle; Bone Marrow Diseases; Chronic Disease; Drug Resistance; Erythropoietin; Follow-Up Studies; Humans; Hyperoxaluria; Immunohistochemistry; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Renal Dialysis; Risk Assessment; Severity of Illness Index; Treatment Failure

The consumption of foods made from soybeans is increasing because of their desirable nutritional value. However, some soy foods contain high concentrations of oxalate and/or phytate. Oxalate is a component of calcium oxalate kidney stones, whereas phytate is an inhibitor of calcium kidney stone formation. Thirty tested commercial soy foods exhibited ranges of 0.02-2.06 mg oxalate/g and 0.80-18.79 mg phytate/g. Commercial soy foods contained 2-58 mg of total oxalate per serving and 76-528 mg phytate per serving. Eighteen of 19 tofu brands and two soymilk brands contained less than 10 mg oxalate per serving, defined as a low oxalate food. Soy flour, textured vegetable soy protein, vegetable soybeans, soy nuts, tempeh, and soynut butter exhibited greater than 10 mg per serving. The correlation between oxalate and phytate in the soy foods was significant (r = 0.71, P < 0.001) indicating that oxalate-rich soy foods also contain higher concentrations of phytate. There also was a significant correlation, based on molar basis, between the divalent ion binding potential of oxalate plus phytate and calcium plus magnesium (r = 0.90, P < 0.001) in soy foods. Soy foods containing small concentrations of oxalate and moderate concentrations of phytate may be advantageous for kidney stone patients or persons with a high risk of kidney stones.

Topics: Kidney Calculi; Oxalates; Phytic Acid; Soy Foods

Dietary oxalate makes a significant contribution to urinary oxalate excretion and, thus, may have a role in calcium oxalate kidney stone formation. Studies have indicated that the ingestion of oxalate rich foods results in transient increases in plasma oxalate concentrations and urinary oxalate excretion. We examined changes in plasma and urinary oxalate following oral crystalline oxalate loading under controlled dietary conditions to further define the renal handling of oxalate by normal adults.. Six normal adult subjects consumed controlled diets of known oxalate content for 1 week before ingesting loads of 0, 2, 4 and 8 mmol of oxalate. Urinary and plasma changes were measured to assess renal oxalate handling. Urinary excretion of proximal tubule derived enzymes and isoprostanes was monitored to assess for renal injury and oxidative stress.. Time and dose dependent changes in plasma oxalate, urinary oxalate and in the clearance ratio of oxalate-to-creatinine were observed. A significant correlation (r=0.43, p <0.001) between the oxalate-to-creatinine clearance ratio and plasma oxalate levels was identified. No changes in urinary markers of oxidative stress or renal injury were observed following the 8 mmol oxalate load.. Oxalate is rapidly absorbed and cleared by the kidney by filtration and secretion following an oral oxalate load. Renal oxalate secretion has a significant role in the renal handling of an oral oxalate load. There is no evidence of acute renal injury or oxidative stress with oral oxalate loads in these experimental conditions.

Topics: Adult; Creatinine; Female; Glomerular Filtration Rate; Humans; Kidney Calculi; Kidney Function Tests; Kidney Tubules, Proximal; Male; Oxalates; Oxidative Stress; Reference Values

While the effect of jejunoileal bypass (JIB) reversal has been well studied regarding hepatic function, there is little information regarding the effect of reversal on renal function and even less data regarding the metabolic urinary stone environment. We evaluated the results of JIB reversal on renal function, the urinary stone milieu and the clinical development of recurrent calculi in affected patients.. From 1995 to 2003, 4 female patients with a mean age of 48.2 years underwent JIB reversal primarily for refractory stone disease. The clinical and metabolic courses prior to and following bypass reversal were reviewed specifically to evaluate renal function, serum and urinary metabolic stone profiles, and clinical stone formation.. At initial presentation following JIB all 4 patients had significantly increased 24-hour urinary oxalate (range 80 to 160 mg, mean 112.5, normal less than 50) and significantly low 24-hour urinary citrate (range 5 to 62 mg, mean 21.5, normal greater than 320). Following reversal 24-hour urinary oxalate normalized to between 31 and 36 mg (mean 33.75). However, 24-hour urinary citrate continued to be low (range 215 to 248 mg, mean 226.5). After JIB reversal all 4 patients continued to have new stones until the commencement of urinary alkalization, following which only 1 had 1 calculus, which occurred 47 months after reversal. After JIB mean serum creatinine was 1.48 mg/dl (range 0.8 to 1.9) and mean urinary creatinine excretion was 0.91 mg per hour (range 0.69 to 1.15). After JIB reversal mean serum creatinine was 1.28 mg/dl (range 0.6 to 2.0) and mean urinary creatinine excretion was 1.0 mg per hour (range 0.85 to 1.10).. JIB reversal normalizes 24-hour urinary oxalate. While urinary citrate improves, it continues to be low and such patients are at high risk for recurrent stone formation. However, in this setting appropriate replacement therapy has a significant and positive impact on that propensity.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Follow-Up Studies; Humans; Intestinal Absorption; Jejunoileal Bypass; Kidney Calculi; Kidney Function Tests; Oxalates; Probability; Reoperation; Risk Assessment; Sampling Studies; Severity of Illness Index; Treatment Outcome; Urinary Calculi

Exposure to oxalate, a constituent of the most common form of kidney stones, generates toxic responses in renal epithelial cells, including altered membrane surface properties and cellular lipids, changes in gene expression, disruption of mitochondrial function, formation of reactive oxygen species and decreased cell viability. Oxalate exposure activates phospholipase A2 (PLA2), which increases two lipid signaling molecules, arachidonic acid and lysophosphatidylcholine (Lyso-PC). PLA2 inhibition blocks, whereas exogenous Lyso-PC or arachidonic acid reproduce many of the effects of oxalate on mitochondrial function, gene expression and cell viability, suggesting that PLA2 activation plays a role in mediating oxalate toxicity. Oxalate exposure also elicits potentially adaptive or protective changes that increase expression of proteins that may prevent crystal formation or attachment. Additional adaptive responses may facilitate removal and replacement of dead or damaged cells. The presence of different inflammatory cells and molecules in the kidneys of rats with hyperoxaluria and in stone patients suggests that inflammatory responses play roles in stone disease. Renal epithelial cells can synthesize a variety of cytokines, chemoattractants and other molecules with the potential to interface with inflammatory cells; moreover, oxalate exposure increases the synthesis of these molecules. The present studies demonstrate that oxalate exposure upregulates cyclooxygenase-2, which catalyzes the rate-limiting step in the synthesis of prostanoids, compounds derived from arachidonic acid that can modify crystal binding and may also influence inflammation. In addition, renal cell oxalate exposure promotes rapid degradation of IkappaBalpha, an endogenous inhibitor of the NF-kappaB transcription factor. A similar response is observed following renal cell exposure to lipopolysaccharide (LPS), a bacterial cell wall component that activates toll-like receptor 4 (TLR4). While TLRs are primarily associated with immune cells, they are also found on many other cell types, including renal epithelial cells, suggesting that TLR signaling could directly impact renal function. Prior exposure of renal epithelial cells to oxalate in vitro produces endotoxin tolerance, i.e. a loss of responsiveness to LPS and conversely, prior exposure to LPS elicits a similar heterologous desensitization to oxalate. Renal cell desensitization to oxalate stimulation may have profound effects on the out

Topics: Animals; Cells, Cultured; Cyclooxygenase 2; Dogs; Epithelial Cells; Humans; Kidney Calculi; Kidney Tubules, Proximal; Lipopolysaccharides; Oxalates; Phospholipases A; Phospholipases A2; Signal Transduction; Toll-Like Receptors; Up-Regulation

The ethanolic extract of Asparagus racemosus Willd. was evaluated for its inhibitory potential on lithiasis (stone formation), induced by oral administration of 0.75% ethylene glycolated water to adult male albino Wistar rats for 28 days. The ionic chemistry of urine was altered by ethylene glycol, which elevated the urinary concentration of crucial ions viz. calcium, oxalate, and phosphate, thereby contributing to renal stone formation. The ethanolic extract, however, significantly (p < 0.05) reduced the elevated level of these ions in urine. Also, it elevated the urinary concentration of magnesium, which is considered as one of the inhibitors of crystallization. The high serum creatinine level observed in ethylene glycol-treated rats was also reduced, following treatment with the extract. The histopathological findings also showed signs of improvement after treatment with the extract. All these observations provided the basis for the conclusion that this plant extract inhibits stone formation induced by ethylene glycol treatment.

Topics: Animals; Asparagus Plant; Calcium; Creatinine; Ethylene Glycol; Kidney; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Plant Extracts; Plant Roots; Rats; Rats, Wistar

Vitamin B6 metabolites and their potential correlates to urinary oxalate excretion in idiopathic calcium stone formers (ICSF) compared with healthy subjects were investigated. This clinical study was performed in a population of male ICSF with (Hyperoxalurics, n=55) or without hyperoxaluria (Normooxalurics, n=57) as well as in 100 healthy male control subjects. Pyridoxal 5'-phosphate serum concentration (S-pyridoxal 5'P) and 24-h urinary excretion of 4-pyridoxic acid (U-4pyridoxic acid) were measured using HPLC; 24-h urinary excretion of oxalate (U-oxalate) was measured concurrently. A subgroup of subjects (40 Hyperoxalurics, 15 Normooxalurics and 50 controls) underwent the same measurements before and after 7-day pyridoxine loading per os (pyridoxine hydrochloride, 300 mg/d). Under usual conditions, U-4pyridoxic acid was similar in the three groups, whereas mean S-pyridoxal 5'P was significantly lower ( p<0.0001) in the Hyperoxalurics (59.6+/-21.2 nmol/L) and in the Normooxalurics (64.9+/-19.7 nmol/L) than in the controls (86.0+/-31.0 nmol/L). No correlation could be found between U-oxalate and U-4pyridoxic acid or S-pyridoxal 5'P. After B6 loading, S-pyridoxal 5'P was still significantly lower in the Hyperoxalurics (415+/-180 nmol/L, p<0.001) and in the Normooxalurics (429+/-115 nmol/L, p=0.036) than in the controls (546+/-180 nmol/L), although there was no difference between groups for U-4pyridoxic acid. No correlation in any group could be found between changes in U-oxalate and changes in U-4pyridoxic acid or S-pyridoxal 5'P. Although there is no vitamin B6 deficiency in ICSF with or without hyperoxaluria, these patients, on average, have lower levels of S-pyridoxal 5'P than healthy subjects. However, this slight decrease does not seem to account for idiopathic hyperoxaluria.

Topics: Adult; Aged; Case-Control Studies; Chromatography, High Pressure Liquid; Cross-Sectional Studies; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates; Pyridoxal Phosphate; Pyridoxic Acid; Pyridoxine; Vitamin B 6

The incidence of renal stone disease in patients receiving topiramate (Topamax) is 2-4 times that expected in the background population. This has been attributed to a weak carbonic anhydrase inhibitor effect, but published data are scant. Following three cases of renal stones in patients receiving topiramate, we evaluated biochemical risk for nephrolithiasis in eight further unselected patients. Most patients demonstrated inadequate urinary acidification and hypocitraturia; in some cases citrate was undetectable. Several patients also had other risk factors for nephrolithiasis, including increased urinary sodium, calcium and oxalate excretion. The biochemical changes induced by topiramate appear highly penetrant. Experience with this drug is relatively short-lived and it is being prescribed for long-term use in (often) relatively young patients. This report highlights the significantly increased metabolic risk of stone formation in patients receiving topiramate.

Topics: Adult; Calcium; Citric Acid; Epilepsies, Partial; Female; Fructose; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Neuroprotective Agents; Oxalates; Risk Factors; Sodium; Topiramate

Most renal stones in humans are composed of calcium oxalate. An increase in urinary oxalate levels has been shown to result in renal epithelial cell injury and crystal retention. However, the underlying mechanisms are unclear. Although the localization of primary stone formation and the associated cells playing the pivotal role in stone formation are still unknown, renal epithelial cells and interstitial cells seem to be involved in this process. The aim of this study was to evaluate the effects of oxalate on distinct renal epithelial and endothelial cells as well as fibroblasts. The first part focused on the toxicity of oxalate on the cells and a potential time- and dose-dependency. In the second part, renal epithelial cells were cultured in a two-compartment model to examine the vulnerability of the tubular or basolateral side to oxalate. LLCPK1, MDCK, renal fibroblast and endothelial cell lines were cultured under standard conditions. In part 1, cells were grown in standard culture flasks until confluent layers were achieved. Sodium oxalate was delivered at final concentrations of 1, 2 and 4 mM to either the apical or basolateral side (plain medium was delivered to the contralateral side). Cell survival was assessed microscopically by trypan blue staining after 1, 2 and 4 h. The influence of oxalate on proliferation and apoptosis induction was also investigated. In the second part, MDCK and LLCPK1 cells were grown in 6-well plates until confluent layers were achieved. Sodium oxalate at the above concentrations was applied, to either the apical or basolateral side and plain medium was delivered to the opposite side. The same protocol was then followed as in part 1. Part 1: sodium oxalate led to a time- and concentration-dependent decline in cell survival that was comparable in LLCPK1 and MDCK. Non-tubular cell lines like fibroblasts and endothelial cells were significantly more vulnerable to oxalate. These observations were reflected by significant impairment to cell proliferation. We could not demonstrate an induction of apoptosis in any cell line. Part 2: both cell lines were more vulnerable to oxalate on the basolateral side. This effect was more pronounced in MDCK cells at high oxalate concentrations (4 mM). Cells are apparently more resistant on the apical (tubular) side. Our results show that sodium oxalate has a negative effect on the growth and survival of renal epithelial cells and, to a greater extent, also fibroblasts and endothelial cells. W

Topics: Animals; Apoptosis; Cell Survival; Cells, Cultured; Disease Models, Animal; Dogs; Dose-Response Relationship, Drug; Kidney Calculi; Kidney Tubules; LLC-PK1 Cells; Oxalates; Probability; Sensitivity and Specificity; Statistics, Nonparametric; Swine; Urothelium

Oxalate induced renal calculi formation and the associated renal injury is thought to be caused by free radical mediated mechanisms. An in vivo model was used to investigate the effect of phycocyanin (from Spirulina platensis), a known antioxidant, against calcium oxalate urolithiasis. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg) and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given, 1h prior to sodium oxalate infusion. An untreated control and drug control (phycocyanin alone) were also included in the study. We observed that phycocyanin significantly controlled the early biochemical changes in calcium oxalate stone formation. The antiurolithic nature of the drug was evaluated by the assessment of urinary risk factors and light microscopic observation of urinary crystals. Renal tubular damage as divulged by urinary marker enzymes (alkaline phosphatase, acid phosphatase and gamma-glutamyl transferase) and histopathological observations such as decreased tubulointerstitial, tubular dilatation and mononuclear inflammatory cells, indicated that renal damage was minimised in drug-pretreated group. Oxalate levels (P < 0.001) and lipid peroxidation (P < 0.001) in kidney tissue were significantly controlled by drug pretreatment, suggesting the ability of phycocyanin to quench the free radicals, thereby preventing the lipid peroxidation mediated tissue damage and oxalate entry. This accounts for the prevention of CaOx stones. Thus, the present analysis revealed the antioxidant and antiurolithic potential of phycocyanin thereby projecting it as a promising therapeutic agent against renal cell injury associated kidney stone formation.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Antioxidants; Bacterial Proteins; Biomarkers; Cyanobacteria; Disease Models, Animal; gamma-Glutamyltransferase; Hyperoxaluria; Kidney; Kidney Calculi; Lipid Peroxidation; Male; Oxalates; Phycocyanin; Rats; Rats, Wistar; Spirulina

Oxalate bioavailability is an important determinant of whether the consumption of a particular food is a high risk in individuals predisposed to kidney stones. We estimated and compared oxalate absorption from a high oxalate containing legume (black beans) and a high oxalate containing nut (almonds). We also compared an isotope method using extrinsically labeled oxalate and an oxalate load method to assess oxalate absorption.. Six male and 5 female subjects participated in the 4 oxalate load tests, namely almonds, almonds with 20 mg C2-oxalic acid, black beans and black beans with 20 mg C2-oxalic acid. Each treatment provided a total of 120 mg oxalate, after which timed urine samples were collected for the analysis of oxalate, calcium and creatinine.. Average oxalate absorption from the 2 almond treatments (5.9%) using the oxalate load method was significantly higher than that from the 2 black bean treatments (1.8%) during the 24-hour post-oxalate load collection period. In contrast, C2-oxalic acid absorption from the almond (7.9%) and black bean (8.6%) treatments did not significantly differ.. The higher oxalate absorption from almonds than from black beans suggests that the relative amount of soluble and insoluble oxalate in food has an important role in the determination of oxalate absorption. Since extrinsically provided C2-oxalate and oxalate naturally occurring in the high oxalate test foods appeared to be differentially absorbed, the data do not support the use of extrinsically labeled oxalate to assess food oxalate absorption.

Topics: Adult; Carbon Isotopes; Creatinine; Fabaceae; Female; Food; Humans; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Oxalic Acid; Prunus

The study compared the effect of urinary calcium with that of oxalate on urinary saturation [relative saturation ratio (RSR)] of calcium oxalate.. A retrospective data analysis was conducted on urinary stone risk analysis from 667 patients with predominantly calcium oxalate stones. Urinary RSR of calcium oxalate was individually calculated using Equil 2. A "theoretical" curve of the relationship between urinary RSR of calcium oxalate and concentration of calcium or oxalate was obtained at two stability constants for calcium oxalate complex, while varying calcium or oxalate and using group mean values for urinary constituents.. At the stability constant of 7.07 x 10(3), the increase in RSR of calcium oxalate was less marked with calcium than with oxalate. However, at the stability constant of 2.746 x 10(3) from the Equil 2 that is considered the "gold standard," calcium and oxalate were equally effective in increasing RSR of calcium oxalate. The above theoretical curves (relating RSR with calcium or oxalate) were closely approximated by the actual curves constructed with data from individual urine samples. Urinary saturation of calcium oxalate was equally dependent on urinary concentrations of calcium and oxalate (r= 0.75 unadjusted and 0.57 adjusted for variables, and P < 0.0001 for calcium; r= 0.73 unadjusted and 0.60 adjusted, P <0.0001 for oxalate).. Among calcium oxalate stone-formers, urinary calcium is equally effective as urinary oxalate in increasing RSR of calcium oxalate.

Topics: Adult; Aged; Calcium; Calcium Oxalate; Humans; Kidney Calculi; Middle Aged; Models, Biological; Osmolar Concentration; Oxalates; Retrospective Studies; Risk Factors

Increased rates of either oxalate absorption or endogenous oxalate synthesis can contribute to hyperoxaluria, a primary risk factor for the formation of calcium oxalate-containing kidney stones. This study involves a comparative assessment of oxalate absorption and endogenous oxalate synthesis in subpopulations of stone formers (SFs) and non-stone formers (NSFs) and an assessment of the effect of ascorbate supplementation on oxalate absorption and endogenous oxalate synthesis.. Twenty-nine individuals with a history of calcium oxalate kidney stones (19 men, 10 women) and 19 age-matched NSFs (8 men, 11 women) participated in two 6-day controlled feeding experimental periods: ascorbate-supplement (2 g/d) and no-supplement treatments. An oxalate load consisting of 118 mg of unlabeled oxalate and 18 mg of 13C2 -oxalic acid was administered the morning of day 6 of each experimental period.. Mean 13C2 -oxalic acid absorption averaged across the ascorbate and no-supplement treatments was significantly greater in SFs (9.9%) than NSFs (8.0%). SFs also had significantly greater 24-hour post-oxalate load urinary total oxalate and endogenous oxalate levels with both treatments. Twenty-four-hour urinary total oxalate level correlated strongly with both 13C2 -oxalic acid absorption (SFs, r = 0.76; P < 0.01; NSFs, r = 0.62; P < 0.01) and endogenous oxalate synthesis (SFs, r = 0.95; P < 0.01; NSFs, r = 0.92; P < 0.01).. SFs are characterized by greater rates of both oxalate absorption and endogenous oxalate synthesis, and both these factors contribute to the hyperoxaluric state. The finding that ascorbate supplementation increased urinary total and endogenous oxalate levels suggested that this practice is a risk factor for individuals predisposed to kidney stones.

Topics: Adult; Aged; Ascorbic Acid; Calcium Oxalate; Female; Humans; Hyperoxaluria; Kidney; Kidney Calculi; Male; Middle Aged; Oxalates

We determined whether dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate treatment, would prevent stone formation and avert bone loss in 18 men and 10 women with type I absorptive hypercalciuria.. Patients were treated with thiazide (20) or indapamide (8) and potassium citrate (average dose 35 mEq. daily) for 1 to 11 years (mean 3.7) while maintained on low calcium oxalate diet. Serum and urinary chemistry studies and bone mineral density were measured at baseline and at the end of treatment. New stones formed were quantitated during 3 years before and during treatment.. During treatment urinary calcium significantly decreased (346 +/- 85 to 248 +/- 79 mg. daily, p <0.001) but urinary oxalate did not change. Urinary pH and citrate significantly increased, and urinary saturation of calcium oxalate significantly decreased by 46%. Stone formation rate decreased significantly from 2.94 to 0.05 per year (p <0.001). L2-L4 bone mineral density increased significantly by 5.7% compared to normal peak value, and by 7.1% compared with normal age and gender matched value. Femoral neck bone mineral density also increased significantly.. Dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate, satisfactorily controlled hypercalciuria, prevented the secondary increase in urinary oxalate, reduced urinary saturation of calcium oxalate, virtually eliminated recurrent stone formation, and increased bone density of the spine and femoral neck. Thus, this dietary pharmacological program controlled stone formation as well as bone loss that often accompany type 1 absorptive hypercalciuria.

Topics: Absorption; Adult; Benzothiadiazines; Bone Resorption; Calcium; Calcium, Dietary; Combined Modality Therapy; Diet; Diuretics; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Potassium Citrate; Sodium Chloride Symporter Inhibitors

Hypercalciuria and hyperoxaluria are important risk factors in the pathogenesis of kidney stones. Urinary glycolate has also been reported to be elevated in patients with renal stones. 1,25-Dihydroxyvitamin D(3), the active metabolite of vitamin D, has been reported to induce hyperoxaluria after either oral or intravenous administration. 1-alpha-D(3), a synthetic derivative of vitamin D, together with ethylene glycol, has been reported to induce renal stones in experimental rats. We have examined the effect of 1-alpha-vitamin D(3) on urinary oxalate and glycolate excretion. Our results indicate that 1-alpha-D(3), together with ethylene glycol, caused a significant increase in urinary glycolate, without a parallel rise in urinary oxalate excretion, in ethylene glycol-fed rats. This increase in urinary glycolate was due to the synergistic effect of both drugs.

Topics: Administration, Oral; Animals; Carbon Radioisotopes; Drug Synergism; Ethylene Glycol; Glycolates; Injections, Intraperitoneal; Kidney Calculi; Male; Oxalates; Rats; Rats, Wistar; Vitamin D

The aim of this study was to evaluate prospectively the influence of nutrition on certain factors which may inhibit or promote nephrocalcinosis in two groups of preterm infants, receiving total parenteral nutrition (TPN) and special preterm milk formula respectively, but not furosemide. A total of 37 preterm infants, 15 on TPN and 22 fed a special preterm formula were studied at the end of the 1st, 2nd and 3rd weeks of life, at which time serum and 8 h urine specimens were collected. High ratios of urinary calcium to urinary creatinine (UCa/cr), urinary oxalate to urinary creatinine (Uox/cr) and urinary calcium to urinary citrate (UCa/cit) indicates an increased risk for nephrocalcinosis while high urinary citrate to urinary creatinine (Ucit/cr) ratio indicates protection. Uox/cr increased significantly (P<0.05) in those infants fed preterm formula, from the end of 2nd week of life and was two-fold higher than in the TPN group of preterm infants (P<0.01). Ucit/cr was higher throughout the study period in the formula fed than in the TPN preterm infants. UCa/cit was five-fold higher (P<0.01) in the TPN group, by the end of the 3rd week. Urinary calcium and magnesium was similar in both groups during the study period. Two of the infants studied (5.4%), one from each group, developed nephrocalcinosis.. In preterm neonates on total parenteral nutrition, urinary oxalate -to-creatinine ratio (a potent lithogenic factor) was lower and urinary citrate -to-creatinine ratio (a lithoprotective factor) also lower than in formula fed neonates. The type of feeding (total parenteral nutrition or special preterm milk formula) seems to affect urinary oxalate and citrate but not calcium and magnesium in non-furosemide treated preterm infants during the first 3 weeks of life.

Topics: Animals; Calcium; Creatinine; Humans; Infant Formula; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Kidney Calculi; Magnesium; Milk; Oxalates; Parenteral Nutrition, Total

To determine the extent of transient changes of tubular function in idiopathic calcium-oxalate (CaOx) stone-bearing patients after extracorporeal shock wave lithotripsy (ESWL), calcium and oxalate excretion were measured before and after ESWL.. In 22 patients with renal CaOx stones, the plasma values and urine excretion of creatinine, calcium, oxalate, magnesium, and citrate were measured before and on days 1 and 2 after ESWL under conditions of a standardized diet. Overnight urine collection for an 8-hour period was used to measure the urine excretion, and the values were extrapolated to a 24-hour period. For calculation of the urine ion activity, the AP(CaOx) index EQ(s) and the CaOx risk index were used.. After ESWL, hyperoxaluria was noted in 10 patients compared with 2 before ESWL. Hypercalciuria was seen in 11 patients after ESWL compared with 3 before. Combined hyperoxaluria and hypercalciuria was found in 7 patients after ESWL compared with 1 before. Both the oxalate/creatinine and calcium/creatinine ratios were significantly increased after ESWL. The AP(CaOx) index EQ(s) and the CaOx risk index were significantly increased after ESWL in patients with increased post-ESWL calcium and/or oxalate excretion.. Increased calcium and/or oxalate excretion can be seen in patients with CaOx stones early after ESWL. This increased excretion of lithogenic substances represents an increased risk of fragment apposition after ESWL for the group with a significantly increased AP(CaOx) index EQ(s) and CaOx risk index. Therefore, prophylactic measures in patients at risk early after ESWL might be warranted to prevent possible recurrent stone formation.

Topics: Adult; Aged; Calcium; Calcium Oxalate; Citrates; Creatinine; Female; Humans; Kidney Calculi; Kidney Tubules; Lithotripsy; Magnesium; Male; Middle Aged; Oxalates; Prospective Studies; Recurrence; Risk

To determine whether lipid peroxidation plays a role in patients with calcium oxalate kidney stones and to determine the correlation of lipid peroxidation with tubular damage and the major urinary risk factors. We also used the isoenzymes of glutathione S-transferase (GST) to examine which parts of the renal tubules were injured in patients with renal stones.. This clinical study included two study groups. Group 1 included 32 normal volunteers, and group 2 included 32 patients with calcium oxalate kidney stones. A 24-hour urine sample was collected from each subject, and the levels of Ca, P, Mg, oxalate, citrate, N-acetyl-beta-glucosaminidase (NAG), beta-galactosidase (GAL), alphaGST, piGST, osteopontin (OPN), thiobarbituric acid-reactive substances (TBARS), and malondialdehyde (MDA) were examined.. Hyperoxaluria, hypocitraturia, and low urinary OPN were the major abnormalities found in the patients with stones. Elevated urinary alphaGST, NAG, and GAL were also noted in the patients with stones; however, urinary piGST showed no statistically significant difference compared with the controls. Urinary TBARS and MDA had statistically significant correlations with alphaGST, GAL, NAG, Ca, and oxalate, but had no correlation with piGST, citrate, OPN, Mg, and P. Urinary citrate had a negative, linear, and statistically significant correlation with alphaGST, GAL, and NAG.. Lipid peroxidation correlated with hyperoxaluria and renal tubular damage, indicating that hyperoxaluria can induce tubular cell injury and that this injury may be due to the production of free radicals in patients with calcium oxalate stones. Renal tubular damage in patients with stones may be limited to the proximal tubules.

Topics: Acetylglucosaminidase; beta-Galactosidase; Biomarkers; Calcium Oxalate; Citric Acid; Female; Glutathione Transferase; Humans; Isoenzymes; Kidney Calculi; Kidney Tubules; Lipid Peroxidation; Magnesium; Male; Malondialdehyde; Middle Aged; Osteopontin; Oxalates; Phosphorus; Risk Factors; Sialoglycoproteins; Thiobarbituric Acid Reactive Substances

The aim of this study was to analyze the frequency of renal stone patients with chronic inflammatory bowel disease and their urinary patterns.. During a 20-year period, 1941 consecutive patients with renal stone disease underwent routine laboratory procedures including a fasting blood sample for chemistry profile and a 24-hour urine collection for analyses of electrolytes. Thorough histories including chronic inflammatory disease or ileal resection were obtained. Patients with inflammatory bowel disease together with a control group comprising 47 idiopathic renal calcium stone formers were submitted to a xylose absorption test for evaluation of intestinal absorption.. We observed 10 patients with Crohn's disease, 12 with ulcerative colitis and one patient with ileal bypass for obesity. Six patients underwent ileal resection and 10 patients total colectomy. Urinary oxalate excretion was significantly higher and urinary citrate lower in stone patients with ileal disease (Ox 60 +/- 23, Cit 113 + 7-118 mg/day) than in idiopathic stone formers (Ox 28.2 +/- 11.5, Cit 381 +/- 205) and stone patients with ulcerative colitis (Ox 20.3 +/- 14.8, Cit 369 +/- 247). Urinary volume was significantly lower in patients with ulcerative colitis. A significant inverse correlation (-0.38, p < 0.01) between oxalate urinary excretion and blood xylose level was found 2 hours after ingestion of xylose. No significant reduction of xylose absorption was demonstrated in both normoxaluric and hyperoxaluric idiopathic stone patients.. Crohn's disease and ulcerative colitis are characterized by recurrent inflammatory involvement of different intestinal segments involving distinctive urinary patterns. Malabosorption associated with ileal disease causes increased oxalate absorption by increasing oxalate solubility in the intestinal lumen and permeability of the colonic mucosa; a reduced citrate excretion is associated in relation to mild acidosis due to the loss of bicarbonate in the liquid stool. In ulcerative colitis, especially if an ileostomy is present, urine are scanty and concentrated, and urine pH falls, leading to uric acid or mixed stones. Mild hyperoxaluria of idiopathic renal stone formers is not related to subtle intestinal malabsorption.

Topics: Adult; Bile Acids and Salts; Calcium; Citrates; Colectomy; Colitis, Ulcerative; Crohn Disease; Diuresis; Female; Humans; Hydrogen-Ion Concentration; Ileum; Inflammatory Bowel Diseases; Intestinal Absorption; Kidney Calculi; Malabsorption Syndromes; Male; Middle Aged; Oxalates; Prevalence; Retrospective Studies; Solubility; Xylose

Since the incidence of renal calculi in the South African black population is extremely rare while in white subjects it occurs at the same rate as elsewhere in the western world, we investigated the possibility that different renal handling mechanisms in response to different dietary challenges might occur in the 2 race groups.. We administered 5 different dietary protocols, including low calcium, high oxalate, vitamin C, high salt and lacto-vegetarian, to 10 healthy male subjects from each race group. We collected 24-hour urine at baseline and after 4 days on the prescribed diet which were analyzed for biochemical and physicochemical risk factors. Dietary intake was controlled throughout the experimental period. A 24-hour dietary recall questionnaire was recorded at baseline and analyzed using food composition tables. Statistical analysis of variance was performed on all the data.. The low calcium diet caused statistically significant changes only in black subjects, which consisted of urinary oxalate increase (0.17 to 0.23 mmol./24 hours, p = 0.01), relative supersaturation of calcium oxalate decrease (1.88 to 0.97, p = 0.03) and relative supersaturation of brushite increase (0.85 to 1.69, p = 0.03). The high oxalate diet caused statistically significant changes in both race groups but these changes were different in the 2 groups. In white subjects urinary pH increased (6.24 to 6.62, p = 0.01), potassium excretion increased (40.01 to 73.49, p = 0.01) and relative supersaturation of brushite increased (1.34 to 2.12, p = 0.05). In black subjects urinary citrate increased (1.94 to 2.99 mmol./24 hours, p = 0.01). Clinically unimportant changes occurred in both race groups after the other 3 diets.. Renal handling of dietary calcium and oxalate in South African black and white subjects is different and may explain the different stone incidence in the 2 race groups.

Topics: Adolescent; Adult; Ascorbic Acid; Black People; Calcium Oxalate; Calcium, Dietary; Diet; Diet, Vegetarian; Humans; Kidney; Kidney Calculi; Male; Oxalates; Racial Groups; Risk Factors; Sodium, Dietary; White People

In this research, screening and central composite experimental designs are used to determine the effect of various factors on the aggregation and dispersion characteristics of previously grown calcium oxalate monohydrate (COM) crystals in artificial urinary environments of controlled variables. The variables examined are pH and calcium, oxalate, pyrophosphate, citrate, and protein concentrations in ultrapure water and artificial urine. Optical density measurements, particle size analysis, optical microscopy, AFM force measurements, and protein adsorption have been used to assess the state of aggregation and dispersion of the COM crystals and to elucidate the mechanisms involved in such a complex system. The data indicate that our model protein, mucin, acts as a dispersant. This is attributed to steric hindrance resulting from the adsorbed mucoprotein. Oxalate, however, promotes aggregation. Interesting interactions between protein and oxalate along with protein and citrate are observed. Such interactions (synergistic or antagonistic) are found to depend on the concentrations of these species. Surface responses for these interactions are presented and discussed in this paper. In summary, solution, surface, and interface chemistries interact in a complex manner in the physiological environment to either inhibit or promote aggregation, and an understanding of such interactions may help determine and control the factors affecting kidney stone formation.

Topics: Adsorption; Calcium; Calcium Oxalate; Citrates; Diphosphates; Dose-Response Relationship, Drug; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Microscopy, Atomic Force; Oxalates; Urine

Topics: Bone Density; Calcium; Calcium Oxalate; Calcium, Dietary; Diet Therapy; Diet, Sodium-Restricted; Dietary Proteins; Humans; Kidney Calculi; Male; Oxalates; Secondary Prevention

Oxalate interaction with renal epithelial cells results in a program of events that include alterations in gene expression, re-initiation of DNA synthesis, cell growth and apoptosis. Our studies focused on understanding the mechanisms involved in the oxalate-induced re-initiation of the DNA synthesis. The effects of oxalate alone or in combination with epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and insulin were investigated to determine whether oxalate utilized the p42/44 mitogen activated protein (MAP) kinase pathway, which is a common pathway used by a majority of the mitogens.. LLC-PK1 cells (a renal epithelial cell line of porcine origin) were exposed to oxalate in the presence or absence of three established growth factors, EGF, insulin and PDGF, and of the transcription/translation inhibitors, actinomycin-D and cycloheximide. DNA synthesis was assessed by [3H]-thymidine incorporation. p42/44 MAP kinase activity was assessed by super-shift analysis as well as by immunocomplex kinase assay.. Exposure of growth-arrested LLC-PK1 cells to oxalate resulted in the re-initiation of the DNA synthesis was abolished by [corrected] pretreatment with transcription/translation inhibitors. Oxalate (1 mmol/L), EGF (50 ng/mL) and insulin (100 ng/mL) stimulated DNA synthesis in growth-arrested LLC-PK1 cells, while PDGF (50 ng/mL) had no effect. Effects of EGF and oxalate on DNA synthesis were additive. In contrast, oxalate and insulin had antagonistic effects on DNA synthesis. Additionally, oxalate did not activate the p42/44 MAP kinase pathway while EGF stimulated this pathway.. These findings demonstrate that oxalate does not activate the p42/44 MAP kinase pathway, and the effects of oxalate are mediated by pathways that are distinct from those of EGF, PDGF and insulin.

Topics: Animals; Apoptosis; Cell Division; DNA; Epidermal Growth Factor; Hyperoxaluria; Hypoglycemic Agents; Insulin; Kidney Calculi; LLC-PK1 Cells; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Oxalates; Platelet-Derived Growth Factor; Protein Biosynthesis; Swine; Transcription, Genetic

Oxalate generation at pH-values above 5.0 and an oxalate-protein binding in acidified plasma would appear to complicate the determination of oxalate in plasma.. To avoid complex sample preparation we used a high-performance liquid chromatographic system with an inline enzyme reactor (HPLC-ER) containing immobilised oxalate oxidase. The detection limit was 0.68 micromol/l. Blood was drawn in lithium-heparin vessels and immediately centrifuged at 4 degrees C. The yielded plasma was ultrafiltered using a Centrisart-I-tube. To inhibit oxalate generation by ascorbic acid, the ultrafiltrate was acidified with 1 mol/l hydrochloric acid during ultrafiltration at 4 degrees C. The liquid thus yielded was used for HPLC-ER analysis. Blood samples were obtained from 133 healthy adults (63 men, 70 women, aged 20-94 years) with no history of renal disorder and from 79 patients (53 men, 26 women, aged 19-77 years) with a history of calcium oxalate stone formation.. Mean plasma oxalate was 2.65 +/- 2.31 micromol/l for healthy subjects and 4.21 +/- 0.56 micromol/l for stone formers.. Analysis yielded no significant differences between males and females. A correlation between age and plasma oxalate was found for the healthy adults (p < 0.001).

Topics: Adult; Aged; Aged, 80 and over; Ascorbic Acid; Calcium Oxalate; Chromatography, High Pressure Liquid; Enzymes, Immobilized; Female; Humans; Indicators and Reagents; Kidney Calculi; Male; Middle Aged; Oxalates; Oxidoreductases; Protein Binding; Ultrafiltration

Topics: Calcium Oxalate; Calcium, Dietary; Diet Therapy; Diet, Sodium-Restricted; Dietary Proteins; Humans; Kidney Calculi; Meat; Oxalates; Secondary Prevention

The inhibitory effect of the root of Cyclea peltata Lam. on nephrolithiasis induced in rats by feeding with ethylene glycolated water (1%) for 35 days was summarized. Ethylene glycol administration led to oxalate stone formation, as indicated by its high level in urine. Complementary to this anion, the cation calcium level in urine was elevated. These two ions may have contributed to the formation of calcium oxalate stones. In addition to high serum potassium, a low serum magnesium level contributed to stone formation. Simultaneous administration of the powdered root of Cyclea peltata resulted in decreased urinary oxalate and calcium. Likewise, serum potassium was lowered and magnesium was elevated. These observations provided the basis for the conclusion that this plant inhibits the stone formation induced by ethylene glycol treatment.

Topics: Animals; Cyclea; Ethylene Glycol; Kidney; Kidney Calculi; Male; Oxalates; Phytotherapy; Plant Roots; Powders; Rats; Rats, Wistar

Dietary calcium lowers the risk of nephrolithiasis due to a decreased absorption of dietary oxalate that is bound by intestinal calcium. The aim of the present study was to evaluate oxaluria in normocalciuric and hypercalciuric lithiasic patients under different calcium intake. Fifty patients (26 females and 24 males, 41 +/- 10 years old), whose 4-day dietary records revealed a regular low calcium intake (

Topics: Adult; Calcium; Calcium, Dietary; Feeding Behavior; Female; Humans; Kidney Calculi; Male; Oxalates

To identify the role of metabolic risk factors in the development of renal calculi associated with ureteropelvic junction obstruction (UPJO) in children.. A metabolic evaluation, including serum biochemistry and measurement of daily urinary calcium, creatinine, oxalate, citrate, magnesium, urate, and inorganic phosphorus, was carried out in three different populations as follows: UPJO group, 12 children with UPJO and coexisting nephrolithiasis (median age 6 years); calcium stone formation (CSF) group, 90 children with normal urologic anatomy and calcium urolithiasis (median age 7 years); control group, 24 healthy children (median age 7.3 years). The investigation data of the three groups were compared.. The stone composition was calcium oxalate in 9 of the 12 children with UPJO. The investigation data of the UPJO group and CSF group were not significantly different. Both groups differed from the control group in a similar manner. The UPJO and CSF groups excreted more oxalate (P = 0.067 and 0.014, respectively) and less citrate (P = 0.020 and 0.010, respectively) than did the control subjects.. Abnormal urinary biochemistry seems to have an additional role in the high incidence of nephrolithiasis in children with upper tract anatomic anomalies, and the urinary biochemistry should be screened in such children.

Topics: Calcium Oxalate; Case-Control Studies; Child; Child, Preschool; Citric Acid; Cross-Sectional Studies; Female; Humans; Kidney Calculi; Male; Oxalates; Prospective Studies; Ureteral Obstruction

Results of a 24-hour urine collection are integral to the selection of the most appropriate intervention to prevent kidney stone recurrence. However, the currently accepted definitions of normal urine values are not firmly supported by the literature. In addition, little information is available about the relationship between risk of stone formation and the levels of urinary factors. Unfortunately, the majority of previous studies of 24-hour urine chemistries were limited by the inclusion of recurrent stone formers and poorly defined controls.. We obtained 24-hour urine collections from 807 men and women with a history of kidney stone disease and 239 without a history who were participants in three large ongoing cohort studies: the Nurses' Health Study I (NHS I; mean age of 61 years), the Nurses' Health Study II (NHS II; mean age of 42 years), and the Health Professionals Follow-up Study (HPFS; mean age of 59 years).. Mean 24-hour urine calcium excretion was higher and urine volume was lower in cases than controls in NHS I (P < or = 0.01), NHS II (P < or = 0.13) and HPFS (P < or = 0.01), but urine oxalate and citrate did not differ. Among women, urine uric acid was similar in cases and controls but was lower in cases in men (P = 0.06). The frequency of hypercalciuria was higher among the cases in NHS I (P = 0.26), NHS II (P = 0.03), and HPFS (P = 0.02), but 27, 17, and 14% of the controls, respectively, also met the definition of hypercalciuria. The frequency of hyperoxaluria did not differ between cases and controls, but was three times more common among men compared with women. After adjusting for the other urinary factors, the relative risk of stone formation increased with increasing urine calcium levels and concentration in all three cohorts but not in a linear fashion. Compared with individuals with a urine calcium concentration of <75 mg/L, the relative risk of stone formation among those with a urine calcium concentration of > or =200 mg/L for NHS I was 4.34 (95% CI, 1.59 to 11.88), for NHS II was 51.09 (4.27 to 611.1), and for HPFS was 4.30 (1.71 to 10.84). There was substantial variation in the relative risks for stone formation for the concentration of other urine factors within the different cohorts.. The traditional definitions of normal 24-hour urine values need to be reassessed, as a substantial proportion of controls would be defined as abnormal, and the association with risk of stone formation may be continuous rather than dichotomous. The 24-hour urine chemistries are important for predicting risk of stone formation, but the significance and the magnitudes of the associations appear to differ by age and gender.

Topics: Adult; Calcium; Citric Acid; Cohort Studies; Female; Follow-Up Studies; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Multivariate Analysis; Oxalates; Potassium; Risk Factors; Uric Acid; Urine

Whether specific metabolic abnormalities are related to nephrolithiasis in patients with medullary sponge kidney (MSK) remains a debated issue. The purpose of this study is to determine metabolic disorders in patients with MSK and nephrolithiasis compared with idiopathic calcium-stone-forming patients. One hundred eighty-four patients with recurrent calcium-stone formations were investigated with regard to metabolic abnormalities. Of these, 22 patients (11.9%; 13 men, 9 women) showed MSK by radiological examination. MSK was defined as a kidney that presented at least three linear or round papillary opacities in the affected papilla on urography. Multiple stones (more than five) existed in both kidneys in all patients with MSK. The remaining 162 patients (109 men, 53 women) were idiopathic calcium-stone formers. Frequencies of low urine volume (urine < 1,500 mL/24 h) and hyperoxaluria (oxalate > 40 mg/24 h) were similar between the groups. Hypercalciuria (men, calcium > 300 mg/24 h; women, calcium of 250 mg/24 h) was found less frequently in the MSK group. The frequency of hypocitraturia (citrate < 300 mg/24 h) was significantly greater in the MSK group than the idiopathic group (77.3% versus 33.9%, respectively). Mean 24-hour urinary excretions of calcium, citrate, uric acid, and magnesium were significantly less in the MSK group. No differences were found in serum calcium, phosphate, and parathyroid hormone levels between the groups. Low urinary excretions of citrate and magnesium are the most typical metabolic disorders that distinguish MSK stone patients from idiopathic calcium-stone-forming patients. In addition to such anatomic abnormalities as ectatic collecting ducts, low levels of urinary inhibitors of stones seem to contribute to the pathogenesis of nephrolithiasis in patients with MSK.

Topics: Calcium; Chlorides; Citrates; Creatinine; Female; Humans; Kidney Calculi; Kidney Medulla; Magnesium; Male; Medullary Sponge Kidney; Middle Aged; Oxalates; Phosphates; Sodium; Uric Acid; Urinary Calculi; Urination

A previously developed method for screening organic acidurias by capillary electrophoresis has been validated for oxalate and citrate measurement in urine. Sample pretreatment is minimum, just acidification and centrifugation. Detection is by direct UV. Validation parameters of the method can be considered adequate. Response is linear for both analytes in standards and samples. The assayed ranges were 200-1,000 mg/l for citrate and 10-200 mg/l for oxalate. Recoveries ranged from 99.4+/-3 to 101.7+/-2.4%, maximum imprecision in oxalate concentration was of 7.6% RSD and limits of detection in samples were 0.67 mg/l for oxalate and 25.9 mg/l for citrate, both lower than the measured values in samples. Identification of increased glyoxylic (oxoacetic acid) and glyceric acids (2,3-dihydroxy propanoic) are also included to facilitate the diagnosis.

Topics: Biomarkers; Citric Acid; Electrophoresis, Capillary; Glyceric Acids; Glyoxylates; Humans; Kidney Calculi; Oxalates; Reproducibility of Results

Consumption of soybeans and food products made from them is increasing because of their desirable nutritional value. However, the oxalate content of seeds from 11 cultivars of soybean showed relatively high levels of total oxalate from 0.67 to 3.5 g/100 g of dry weight. Oxalate primarily was found as calcium oxalate crystals. Thirteen tested commercial soyfoods contained between 16 and 638 mg of total oxalate per serving. These values compare to those of three other legume foods, peanut butter, refried beans, and lentils, which contained 197, 193, and 100 mg of total oxalate per serving, respectively. After oxalate has been absorbed from the diet, it cannot be metabolized and is excreted by the kidney into urine, where it binds to calcium forming an insoluble salt that may precipitate to form kidney stones. The amounts of total oxalate in soybean seeds, soy foods, and other common legume foods exceed current recommendations for oxalate consumption by individuals who have a history of calcium oxalate kidney/urinary stones. This study serves as the basis to find soybean cultivars lower in oxalate, which will have lower risk for kidney stone formation after human consumption.

Topics: Calcium Oxalate; Fabaceae; Food Analysis; Glycine max; Humans; Kidney Calculi; Nutritive Value; Oxalates; Plants, Medicinal; Seeds

An enzymatic method for the determination of pyrophosphate which has been applied to renal calculi is described. The method involves the preconcentration of pyrophosphate using anionic exchange resin and development of the enzymatic reactions with the pyrophosphate retained on the resin. The study of calculi treatment according to calculi composition is also reported. The pyrophosphate content was dependent on the calculi composition. The highest amount of pyrophosphate was found in hydroxyapatite calculi (of the order of 10 microg/g), struvite and oxalate calculi showed a lower amount (the order was 2.5 and 4.5 microg/g, respectively) and was not detected in uric acid and cystine stones. The method was also successfully applied to the determination of pyrophosphate in human urine. For urinary pyrophosphate determination, a modification based on a clean-up of urine using activated carbon has been proposed. Pyrophosphate in human urine was of the order of 4 mg l(-1).

Topics: Algorithms; Cystine; Diphosphates; Fructose-Bisphosphate Aldolase; Humans; Hydrogen-Ion Concentration; Indicators and Reagents; Kidney Calculi; Oxalates; Reference Values; Spectrophotometry, Ultraviolet; Uric Acid

The determination of urinary excretion of lithogenic elements in healthy newborns involves factors ranging from urine collection and data handling to maternal influences, which can cause difficulties in analyzing the results. The objective of this study was to determine normal values of parameters related to lithogenesis, such as calcium, uric acid, citrate, and oxalate, in urine of healthy newborns using isolated samples, focusing on variations according to gender, weight, milk ingestion, and family history of lithiasis. Parameters measured in isolated urine samples from 104 healthy newborns (77 males and 27 females) were corrected by creatinine. The ratios were expressed as milligram/milligram of creatinine: calcium/creatinine of 0.10+/-0.01 (X+/-SE), uric acid/ creatinine of 1.10+/-0.10, citrate/creatinine of 0.56+/-0.04, and oxalate/creatinine of 0.07+/-0.01. Differences were observed between males and females, in terms of uric acid (0.80+/-0.07 vs. 1.10+/-0.10 mg/mg, P<0.05), citrate (0.05+/-0.06 vs. 0.17+/-0.05, P<0.05), sodium (0.17+/- 0.01 vs. 0.05+/-0.01, P<0.001), and potassium (0.05+/- 0.01 vs. 0.20+/-0.02, P<0.001). Interestingly, the urinary concentration of protector factors such citrate and potassium was higher in females than in males with low sodium excretion. Artificial milk feeding leads to higher calcium (0.10+/-0.06 vs. 0.06+/-0.01), uric acid (1.40+/-0.20 vs. 0.90+/-0.09, P<0.05), citrate (0.90+/-0.09 vs. 0.50+/-0.04, P<0.001), and oxalate (0.17+/-0.03 vs. 0.05+/-0.01, P<0.001) excretion when compared with breast feeding. There was higher excretion of calcium and sodium in patients under 3 kg. Children with familial antecedents presented some differences in urinary excretion, with higher uric acid (1.50+/-0.30 vs. 0.80+/-0.08, P<0.05) but lower calcium (0.05+/-0.02 vs. 0.10+/-0.01, P<0.05) and sodium (0.15+/-0.02 vs. 0.20+/-0.02, P<0.05) excretion, respectively. This report provides urinary parameters obtained in healthy newborns and correlates them with factors that could be involved in the genesis of osteopenia, renal stones, and/or nephrocalcinosis.

Topics: Breast Feeding; Calcium; Citrates; Creatinine; Female; Humans; Infant Food; Infant, Newborn; Kidney Calculi; Male; Oxalates; Reference Values; Sex Characteristics; Uric Acid

To examine the influence of dietary intake on urinary oxalate excretion in calcium oxalate stone formers in their forties.. Dietary intake was recorded by using the dietary-record method in 58 idiopathic stone formers in their forties. The patients collected their urine for 24 h at home and their urinary oxalate excretion was measured. The relationship between the dietary intake of various nutrients and urinary oxalate excretion was examined by mono- and multivariate analysis.. The intake of animal fat was correlated with urinary oxalate excretion by monovariate analysis, but that of total protein, animal protein, calcium and carbohydrate were not. By multivariate analysis, the intake of animal fat was correlated with urinary oxalate excretion and the intake of calcium was inversely correlated with urinary oxalate excretion.. The intake of animal fat was positively and the intake of calcium was negatively correlated with the urinary oxalate excretion in stone formers in their forties. It was shown that animal fat plays an important role in urinary oxalate excretion.

Topics: Adult; Age Factors; Calcium Oxalate; Calcium, Dietary; Dietary Fats; Eating; Humans; Kidney Calculi; Male; Oxalates

Topics: Biological Availability; Humans; Kidney Calculi; Oxalates; Tea

Topics: Ascorbic Acid; Dietary Supplements; Female; Humans; Kidney Calculi; Male; Oxalates; Risk Factors

We studied the relationship of stone frequency and composition to age, sex and stone weight.. A retrospective study was performed of all 15,624 stones submitted for analysis with infrared and wet chemical methods in Newfoundland and Labrador from 1979 to 1998.. There were 1,067 bladder stones of which 216 contained magnesium ammonium phosphate. The remaining 14,557 stones were from the kidney and ureter, and 11,707 were composed only of calcium oxalate and/or phosphate. Of the remaining 2,850 kidney and ureter stones magnesium ammonium phosphate was present in 573, uric acid/urate without magnesium ammonium phosphate in 1,109 and other compounds in 1,168. The 11,707 oxalate phosphate group was subdivided by infrared peak analysis based on oxalate-to-phosphate ratio into phosphate-ratio 1 or less, intermediate-1 to 10 and oxalate-10+. Oxalate comprised 65% of the 11,707 stones compared to 16% for phosphate. Women submitted 52% of phosphate stones compared with 28% of oxalate stones. From the first (1980 to 1983) to the last (1995 to 1998) complete 4-year study periods, there was a relative increase in oxalate and decrease in phosphate stones, associated with increasing age from decades 5 to 6 for oxalate and phosphate stones, except that the age peak for phosphate stones in women remained in decade 3. Median weight of 1, 828 phosphate stones was 43 mg. (mean 234) compared with 25 mg. (mean 98) for 7,634 oxalate stones. Male-to-female ratio was 0.91 for phosphate stones compared with 2.62 for oxalate stones.. Phosphate stones were on average heavier and relatively more common in women, had an earlier age peak frequency in women than oxalate stones and became less frequent during our last 4-year study period. In contrast, oxalate stones were much more common, of lighter weight and became more frequent with time.

Topics: Adolescent; Adult; Age Factors; Aged; Child; Female; Humans; Kidney Calculi; Magnesium Compounds; Male; Middle Aged; Oxalates; Phosphates; Retrospective Studies; Sex Factors; Struvite; Ureteral Calculi; Urinary Bladder Calculi; Urinary Calculi

Exposure to high levels of oxalate induces oxidant stress in renal epithelial cells and produces diverse changes in cell function, ranging from cell death to cellular adaptation, as evidenced by increased DNA synthesis, cellular proliferation, and induction of genes associated with remodeling and repair. These studies focused on cellular adaptation to this oxidant stress, examining the manner by which oxalate exposure leads to increased expression of immediate early genes (IEGs). Specifically, our studies assessed the possibility that oxalate-induced changes in IEG expression are mediated by phospholipase A2 (PLA2), a common pathway in cellular stress responses.. Madin-Darby canine kidney (MDCK) cells were exposed to oxalate in the presence or absence of PLA2 inhibitors: mepacrine and arachidonyl trifluoromethyl ketone (AACOCF3). Expression of IEG (c-jun, egr-1, and c-myc) mRNA was assessed by Northern blot analysis. PLA2 activity was determined by measuring the release of [3H]arachidonic acid (AA) from prelabeled cells.. Oxalate exposure (1 to 1.5 mmol/L) induced time- and concentration-dependent increases in IEG mRNA. Treatment with mepacrine resulted in a 75 to 113% reduction of oxalate-induced c-jun, egr-1, and c-myc mRNA, while AACOCF3 caused a 41 to 46% reduction of oxalate-induced c-jun and egr-1 mRNA. Of the two major byproducts of PLA2, only lysophosphatidylcholine (20 micromol/L) increased c-jun and egr-1 mRNA. In contrast, AA (25 micromol/L) attenuated the oxalate-induced increase in c-jun and egr-1 mRNA, presumably by inhibiting PLA2 activity.. These findings suggest that PLA2 plays a major role in oxalate-induced IEG expression in renal epithelial cells and that lysophospholipids might be a possible lipid mediator in this pathway.

Topics: Animals; Apoptosis; Arachidonic Acid; Arachidonic Acids; Blotting, Northern; Calcimycin; Cells, Cultured; DNA-Binding Proteins; Dogs; Enzyme Inhibitors; Epithelial Cells; Gene Expression Regulation, Enzymologic; Genes, Immediate-Early; Ionophores; Kidney; Kidney Calculi; Lysophospholipids; Oxalates; Oxidative Stress; Phospholipases A; Phospholipases A2; Proto-Oncogene Proteins c-jun; Proto-Oncogene Proteins c-myc; Quinacrine; RNA, Messenger; Transcription Factors; Tritium

Increased arachidonic acid content in red blood cell membranes of stone formers (SF) has recently been reported and is hypothesized as representing the underlying causal factor for both hyperoxaluria and hypercalciuria. We performed the present study to see whether we could confirm this finding and to test whether any relationship exists between the fatty acid composition of red blood cell membranes and the main metabolic factors involved in stone formation.. In 21 SF and 40 healthy controls subjects the fatty acid composition of red blood cell membranes was assessed. In addition, the following parameters were evaluated in SF: daily and fasting urinary calcium excretion, fractional intestinal calcium absorption, 1,25-dihydroxy-vitamin D, intact parathyroid hormone, hydroxyproline in fasting urine, daily urinary excretion of oxalate, citrate, urate, electrolytes, urea, sulphate, relative supersaturation for calcium oxalate monohydrate.. The red blood cell membrane of SF had a lower content of arachidonic acid, linoleic acid, and docosahexaenoic acid than that of control subjects. Arachidonic acid content was not correlated with any of the parameters studied. However, when patients were grouped according to the degree of oxalate excretion, hyperoxaluric SF had a higher arachidonic acid content and arachidonic/linoleic acid ratio than SF with normal oxalate excretion.. Our results do not confirm the finding of an increased arachidonic acid content of red blood cell membrane in SF. On the contrary, reduced arachidonic acid levels were found in our patients. However, hyperoxaluric SF had a relatively higher arachidonic acid content than SF with normal urinary oxalate excretion.

Topics: Adult; Arachidonic Acid; Calcium; Docosahexaenoic Acids; Erythrocyte Membrane; Fatty Acids; Female; Humans; Intestinal Absorption; Kidney Calculi; Linoleic Acid; Male; Middle Aged; Oxalates; Reference Values

The aim of the study was to measure urinary excretion of Tamm-Horsfall protein (THP), an important inhibitor of crystallization, and to identify possible determinants of urinary THP excretion in non-selected kidney stone formers (SF) and healthy subjects (C).. By means of a commercially available ELISA (Pharmacia and Upjohn/Elias, Germany), we measured THP in 24-h urines of 104 SF (74 males/30 females, age 16-74 years) who had formed 8.7+/-2.4 stones (range 1-240), and of 71 C (41 males/30 females, age 22-62 years). Types of stones formed by SF were 88 calcium, eight uric acid, six infection, and two cystine. All values are means+/-SE.. The normal range (5th to 95th percentile) of U(THP)xV was 9.3-35.0 mg/day in males and 9.0-36.3 mg/day in females respectively. Mean U(THP)xV was 21.3+/-1.2 mg/day (range 3. 4-51.6) in male and 15.2+/-1.6 mg/day (range 1.8-32.3) in female SF (P=0.008 vs male SF). Since U(THP)xV was positively correlated with C(Crea) (r=0.312, P=0.001) in SF as well as with U(Crea)xV (r=0.346, P=0.0001) and with body surface (r=0.271, P=0.0003) in all study subjects, mean THP/Crea (mg/mmol) was used for all further calculations. Overall, THP/Crea was lower in SF (1.42+/-0.07 vs 1. 68+/-0.08, P:=0.015), mainly due to increased THP/Crea in female C (2.08+/-0.11, P=0.0036 vs female SF, P=0.0001 vs male C and vs male calcium SF), which also explains decreased THP/Crea values in calcium SF (1.46+/-0.08, P=0.041 vs C). In addition, THP/Crea was reduced in uric acid SF (1.11+/-0.21, P=0.049 vs C). Whereas THP/Crea was not related to age, urine volume, intake of dairy calcium, or urinary markers of protein intake, either in C or in SF, it correlated significantly with urinary Citrate/Crea, both in C (r=0.523, P=0.0001) and in SF (r=0.221, P=0.025). In C only, but not in SF, THP/Crea was correlated with urinary Calcium/Crea (r=0. 572, P=0.0001) and with Oxalate/Crea (r=0.274, P=0.022).. Both in C and SF, urinary THP excretion is related to body size, renal function and urinary citrate excretion, whereas dietary habits apparently do not affect THP excretion. Uric acid and calcium stone formation predict reduced THP excretion in comparison with C, whereas female gender goes along with increased urinary THP excretion in C. Possibly most relevant to kidney stone formation is the fact that THP excretion rises only in C in response to increasing urinary calcium and oxalate concentrations, whereas this self-protective mechanism appears to be missing in SF.

Topics: Adult; Body Constitution; Calcium; Citric Acid; Female; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Mucoproteins; Oxalates; Prospective Studies; Reference Values; Sex Characteristics; Uric Acid; Uromodulin

Many studies on the etiology of stone disease have focused on the properties of urine that affect crystal nucleation and growth. More recent studies have focused on the properties of the renal epithelium and the role of injury in crystal retention. The latter studies have shown that oxalate exposure per se can damage renal epithelial cells and enhance crystal binding. This overview summarizes findings of specific biochemical and genetic alterations observed in renal epithelial cells after exposure to oxalate. In LLC-PK1 and MDCK cells, oxalate exposure produces marked effects on membranes, causing a redistribution of phosphatidylserine and activation of two lipid signaling cascades, one involving phospholipase A(2) (PLA(2)) and one involving ceramide. Longer exposure to oxalate leads to membrane damage and cell death. Adaptive responses are also observed, including proliferation (for replacement of damaged cells) and induction of various genes (for cellular replacement and repair). Many or all of these responses are blocked by antioxidants, and many can be mimicked by PLA(2) agonists/products. This finding suggests links between oxalate-induced increases in oxidant stress, lipid signaling pathways, and subsequent molecular responses that may eventuate in renal cell damage or death. Whether such changes play a role in stone disease in vivo, and whether strategies to inhibit these changes would be beneficial therapeutically, is unknown.

Topics: Animals; Antioxidants; Arachidonic Acid; Blotting, Northern; Cell Division; Cell Line; Cell Membrane; Ceramides; Clusterin; DNA-Binding Proteins; Dogs; Dose-Response Relationship, Drug; Epithelial Cells; Glycoproteins; Kidney; Kidney Calculi; Molecular Chaperones; Osteopontin; Oxalates; Phosphatidylserines; Phospholipases A; Proto-Oncogene Proteins c-myc; RNA, Messenger; Sialoglycoproteins; Signal Transduction; Sphingomyelins; Swine; Time Factors; Transcription Factors

The effects of calcium supplementation on urinary oxalate excretion was tested in 9 normal subjects, 4 males and 5 females between 23 and 49 years of age. In a crossover study 800 mg calcium was orally administered as active absorbable algal calcium (AAACa) (A) and calcium carbonate (B), and compared with non-calcium containing placebo (C). Calcium, oxalate, osmolality, creatinine and pH were measured in the first three morning urine samples and Ca/osmolality, Ca/osmolality/body weight, Ca/creatinine and oxalate/osmolality were calculated to correct for urine dilution. Ca x oxalate product was also calculated and Ca oxalate crystal in the sediment was microscopically examined and semiquantitatively estimated as -, +, ++, and +++ expressed as 0, 1, 2 and 3 respectively. Urinary Ca excretion was similar in A and B, but significantly larger than C, regardless of the method of correction for dilution. Urinary oxalate excretion tended to be lower in A than in B and C. Urine pH was similar among all three groups. Ca x oxalate product was higher in C than in A and B. AAACa, unlike calcium carbonate, appeared to decrease urinary oxalate excretion and Ca x oxalate product more efficiently than Ca carbonate, suggesting a possibility of inhibiting the formation of Ca x oxalate kidney stones. Formation of calcium oxalate was also tested in vitro by adding oxalate to urine samples and aqueous calcium solution.

Topics: Administration, Oral; Adult; Calcium; Calcium Carbonate; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

High dietary protein intake is a potential risk factor for nephrolithiasis because of its capacity to increase urinary calcium and to facilitate lithogenesis through many other mechanisms.. Our aim was to verify the effects of moderate protein restriction in hypercalciuric patients.. We studied 18 patients (10 men and 8 women aged 45.6+/-12.3 y) with idiopathic hypercalciuria and renal calculi. Before and after 15 d of a diet with 0.8 g protein x kg(-1) x d(-1) and 955 mg Ca, all patients were evaluated for the main serum and urinary measures of calcium metabolism as well as for urinary uric acid, oxalate, citrate, and prostaglandin E2.. Urinary excretion of urea fell after the diet (P < 0.001). Urinary calcium (P < 0.001), uric acid (P < 0.005), oxalate (P < 0.01), and hydroxyproline (P < 0.01) decreased after protein restriction, whereas urinary citrate increased (P < 0.025). Blood pH increased after the hypoproteic diet (P < 0.05). 1,25-Dihydroxycholecalciferol (calcitriol) concentration fell significantly (P < 0.025) and parathyroid hormone increased (P < 0.001). Creatinine clearance tended to decrease (106.4+/-4.8 compared with 97.5+/-5.7 mL/min) after the diet. The decrease in urinary uric acid after the diet correlated with calcitriol concentration (r = 0.57, P < 0.05) and the decrease in urinary urea correlated positively with that in hydroxyproline excretion (r = 0.58, P < 0.01).. In hypercalciuric patients, moderate protein restriction decreases calcium excretion, mainly through a reduction in bone resorption and renal calcium loss; both are likely due to a decreased exogenous acid load. Moreover, dietary protein restriction ameliorates the entire lithogenic profile in these patients.

Topics: Calcium; Citric Acid; Diet, Protein-Restricted; Dinoprostone; Female; Humans; Hydroxyproline; Kidney Calculi; Male; Oxalates; Recurrence; Regression Analysis; Risk Factors; Uric Acid

The cluster analysis technique is considered for classifying kidney stones based on data for nine chemical analysis parameters. A set of 214 stones is used, which has been previously classified using empirical classification rules into three stone types using the percentage concentrations of the urate, oxalate, and phosphate radicals. We investigate whether cluster analysis utilising data on all parameters leads to different classifications and explore the possibility of other effective classifiers. We also compare the performance of various clustering techniques, distance and similarity measures and data standardisation methods. Results indicate that inclusion of the additional six parameters does not improve the classification accuracy. Best matching with the empirical classification (6% error) is achieved using the average linkage (between groups) clustering method and the squared Eculidean distance measure without data standardisation. Excluding these three main radicals causes a 63% matching error. Cluster analysis results suggest that carbon ions alone provide a single classifier for the three stone types, giving a matching error of approximately 10% with the empirical classification.

Topics: Cluster Analysis; Humans; Ions; Kidney Calculi; Oxalates; Phosphates; Uric Acid

Urinary oxalate is an important determinant of calcium oxalate kidney stone formation. High doses of vitamin B6 may decrease oxalate production, whereas vitamin C can be metabolized to oxalate. This study was conducted to examine the association between the intakes of vitamins B6 and C and risk of kidney stone formation in women. The relation between the intake of vitamins B6 and C and the risk of symptomatic kidney stones were prospectively studied in a cohort of 85,557 women with no history of kidney stones. Semiquantitative food-frequency questionnaires were used to assess vitamin consumption from both foods and supplements. A total of 1078 incident cases of kidney stones was documented during the 14-yr follow-up period. A high intake of vitamin B6 was inversely associated with risk of stone formation. After adjusting for other dietary factors, the relative risk of incident stone formation for women in the highest category of B6 intake (> or =40 mg/d) compared with the lowest category (<3 mg/d) was 0.66 (95% confidence interval, 0.44 to 0.98). In contrast, vitamin C intake was not associated with risk. The multivariate relative risk for women in the highest category of vitamin C intake (> or =1500 mg/d) compared with the lowest category (<250 mg/d) was 1.06 (95% confidence interval, 0.69 to 1.64). Large doses of vitamin B6 may reduce the risk of kidney stone formation in women. Routine restriction of vitamin C to prevent stone formation appears unwarranted.

Topics: Adult; Age Distribution; Ascorbic Acid; Cohort Studies; Confidence Intervals; Data Collection; Female; Humans; Incidence; Kidney Calculi; Middle Aged; Multivariate Analysis; Oxalates; Prospective Studies; Pyridoxine; Risk Assessment; United States

LLC-PK1 cells were cultured on a permeable support in a two-compartment culture system. Confluent monolayers received an ultrafiltrate-like solution at the apical side and a plasma-like solution at the basolateral side. The distribution of various solutes, including phosphate, calcium, and oxalate over both compartments was measured in time. The transport of water was monitored by alterations in fluid concentrations of radiolabeled inulin. Bicarbonate, glucose, and phosphate were transported rapidly from the apical to basolateral side of the monolayer. Sodium and chloride were reabsorbed without major consequences for the osmolality in the apical and basal fluid. Calcium and potassium were also reabsorbed, but to a smaller extent than sodium. The luminal concentration of oxalate gradually increased to values that were at least three times higher (12.0+/-0.4 micromol/l) than those in the contraluminal fluid (3.8+/-0.1 micromol/l). However, since the luminal rise of oxalate completely matched the rise of inulin in the apical fluid this appeared to be the passive consequence of active water reabsorption rather than of net directed oxalate transport. The LLC-PK1 model could prove useful to study the regulation of proximal tubule water transport and its effect on luminal stone salt concentrations under different physiological conditions.

Topics: Animals; Biological Transport; Electrolytes; Inulin; Kidney Calculi; Kidney Tubules, Proximal; LLC-PK1 Cells; Osmolar Concentration; Oxalates; Swine; Time Factors; Water

The effects of female sex hormones on urinary stone formation are not known. This study was conducted to investigate the effects of these hormones on stone formation by using an ethylene glycol (EG) and vitamin D-induced rat urolithiasis model.. Adult female Wistar rats were fed the same diet for four weeks and were then divided into four groups (N = 10 each). One group was administered 0.5 ml of olive oil three times per week for four weeks as a control. The other three groups were administered 0. 5 microg of vitamin D3 and 0.5 ml of 5% EG three times per week for four weeks. The rats in two of these three groups were oophorectomized, and the rats of the remaining group underwent a sham operation on the day before the start of the four-week treatment period. One of the two oophorectomized groups was then administered a supplementation of female sex hormones (0.1 mg of estrogen and 2.5 mg of progesterone 3 times per week for 4 weeks). On the first day of the fifth week of the experimental period, the degree of crystal deposition was determined histologically, and the calcium content in renal tissue was measured. We also investigated the level of osteopontin (OPN) mRNA in renal tissues by Northern blot analysis. OPN is a matrix protein thought to be a promoter of stone formation.. The urinary oxalate excretion, crystal deposition and calcium content in renal tissue and the expression of OPN-mRNA were greater in the oophorectomized rats compared with the controls, and the same parameters were inhibited by the female sex hormone supplementation.. These results suggest that female sex hormones can inhibit renal crystal deposition in EG-treated rats by suppressing the urinary oxalate excretion and the expression of OPN.

Topics: Animals; Blotting, Northern; Calcium; Citric Acid; Crystallization; Disease Models, Animal; Estradiol; Ethylene Glycol; Female; Kidney Calculi; Kidney Medulla; Kidney Tubules, Distal; Magnesium; Osteopontin; Ovariectomy; Oxalates; Phosphoproteins; Rats; Rats, Wistar; RNA, Messenger; Sialoglycoproteins; Vitamin D

Greater arachidonic acid (AA) contents, which were correlated with erythrocyte transmembrane oxalate (Ox) transport, were observed in plasma and erythrocyte membrane phospholipids of patients with idiopathic calcium renal stones, suggesting a link between membrane phospholipid fatty acid composition and cellular Ox transport. To confirm this hypothesis, the effects of exogenous red blood cell incorporation of three different fatty acids (i.e., oleic acid, AA, and eicosapentaenoic acid) on Ox transport and the phosphorylation status of band 3 protein, which has been shown to mediate red blood cell Ox flux, were investigated. Preincubation of erythrocytes with AA induced a dose-dependent increase in the phosphorylation level of band 3 protein and an increase in transmembrane Ox self-exchange. In contrast, inhibitory effects on both parameters were observed after the incorporation of oleic and eicosapentaenoic acids. These data, together with previous observations of dietary effects on erythrocyte Ox transport and urinary Ox excretion, indicate that genetic and/or nutritional changes in membrane phospholipid fatty acid composition play a crucial role in modulating cellular Ox transport in idiopathic calcium Ox nephrolithiasis.

Topics: Adult; Arachidonic Acid; Biological Transport; Calcium Oxalate; Erythrocytes; Humans; Kidney Calculi; Oxalates

Little is known about the epidemiology of renal stones, in spite of the relative frequency of this painful condition. This population-based study examined reported renal stone diagnosis in 1,309 women aged 20-92 years to determine whether renal stones are associated with 1) food or water exposures or 2) lower bone mineral density and an increased likelihood of fractures. Results indicated a renal stone prevalence of 3.4%. The average age at diagnosis was 42 years. Renal stone formation was not associated with community of residence, hypertension, bone mineral density, fractures, high-oxalate food consumption, or ascorbic acid from food supplements. Women with renal stones consumed almost 250 mg/day less dietary calcium (p < 0.01) than did women without stones and had a lower energy intake (p < 0.04). The authors' findings do not support the hypothesis that increased dietary calcium is associated with a greater prevalence of renal stones, nor do they identify renal stones as a risk factor for low bone mineral density. Furthermore, lack of other identifiable environmental correlates and the relatively young age at initial diagnosis suggest that genetic components of renal stone formation need further study.

Topics: Adult; Age Distribution; Aged; Aged, 80 and over; Alcohol Drinking; Bone Density; Calcium; Energy Metabolism; Feeding Behavior; Female; Fractures, Bone; Humans; Iowa; Kidney Calculi; Life Style; Middle Aged; Oxalates; Prevalence; Risk Assessment; Smoking; Water Supply

Medical records of 56 patients who had undergone jejunoileal bypass (JIB) surgery because of morbid obesity were reviewed. The follow-up time varied from 3 to 25 years (average 16 years). Twenty-two of the 56 patients (39.3%) were found to have renal calculi. The interval between the operation and the occurrence or knowledge of the first stone formation ranged from some months to 19 years. The mean weight loss at 5 years was 36.5 kg. Renal function investigations showed no evidence that the jejunoileal bypass operation alters the renal function. The urinary excretion of oxalate was high: 1.112 mumol/24 h (normal range: 55-400 mumol/24 h), and citrate excretion was low: 1.48 mmol/24 h (normal range: 2-5 mmol/24 h). There was no difference in these respects between stone formers and non-stone formers.

Topics: Adult; Aged; Citric Acid; Female; Follow-Up Studies; Humans; Jejunoileal Bypass; Kidney Calculi; Kidney Function Tests; Male; Middle Aged; Oxalates; Postoperative Complications; Reference Values; Retrospective Studies; Weight Loss

We studied the effect of oral calcium supplementation in patients with enteric hyperoxaluria. Three patients with renal stone events following ileal resection were given oral calcium supplement. One of the three patients was put on a low-fat diet. The treatment reduced urinary oxalate excretion to the normal range. Subsequently, 2 patients reduced the dose of calcium supplementation at their own discretion and consequently developed renal stones again together with hyperoxaluria. Based on these observations, we believe that an adequate dose of calcium can normalize urinary oxalate excretion.

Topics: Administration, Oral; Adult; Calcium; Colectomy; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Humans; Hyperoxaluria; Intestinal Obstruction; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence; Treatment Outcome

Calcium intake is believed to play an important role in the formation of kidney stones, but data on the risk factors for stone formation in women are limited.. To examine the association between intake of dietary and supplemental calcium and the risk for kidney stones in women.. Prospective cohort study with 12-year follow-up.. Several U.S. states.. 91,731 women participating in the Nurses' Health Study I who were 34 to 59 years of age in 1980 and had no history of kidney stones.. Self-administered food-frequency questionnaires were used to assess diet in 1980, 1984, 1986, and 1990. The main outcome measure was incident symptomatic kidney stones.. During 903,849 person-years of follow-up, 864 cases of kidney stones were documented. After adjustment for potential risk factors, intake of dietary calcium was inversely associated with risk for kidney stones and intake of supplemental calcium was positively associated with risk. The relative risk for stone formation in women in the highest quintile of dietary calcium intake compared with women in the lowest quintile was 0.65 (95% CI, 0.50 to 0.83). The relative risk in women who took supplemental calcium compared with women who did not was 1.20 (CI, 1.02 to 1.41). In 67% of women who took supplemental calcium, the calcium either was not consumed with a meal or was consumed with meals whose oxalate content was probably low. Other dietary factors showed the following relative risks among women in the highest quintile of intake compared with those in the lowest quintile: sucrose, 1.52 (CI, 1.18 to 1.96); sodium, 1.30 (CI, 1.05 to 1.62); fluid, 0.61 (CI, 0.48 to 0.78); and potassium, 0.65 (CI, 0.51 to 0.84).. High intake of dietary calcium appears to decrease risk for symptomatic kidney stones, whereas intake of supplemental calcium may increase risk. Because dietary calcium reduces the absorption of oxalate, the apparently different effects caused by the type of calcium may be associated with the timing of calcium ingestion relative to the amount of oxalate consumed. However, other factors present in dairy products (the major source of dietary calcium) could be responsible for the decreased risk seen with dietary calcium.

Topics: Absorption; Adult; Calcium, Dietary; Dietary Sucrose; Female; Follow-Up Studies; Food, Fortified; Humans; Incidence; Kidney Calculi; Middle Aged; Multivariate Analysis; Oxalates; Prospective Studies; Risk Factors; Sodium, Dietary; Surveys and Questionnaires

1. Dietary calcium restriction, an efficient practice in reducing urinary calcium excretion, has been reported to induce either an increase or no change in oxalate excretion, questioning its use in hypercalciuric stone-forming patients. In addition, calcium restriction has been previously demonstrated to induce other urinary changes which might influence the relative supersaturation of calcium oxalate. So the overall effect of calcium deprivation on the relative supersaturation of calcium oxalate is unpredictable. 2. The aim of the study was to evaluate the effect of dietary calcium restriction on the relative supersaturation of calcium oxalate in the urine of stone-forming patients utilizing a computer methodology which takes into account the main soluble complex species of oxalate. 3. We studied 34 stone-forming patients on both a free-choice diet, whose Ca and oxalate content (24 and 1.2 mmol respectively) was assessed by dietary inquiry, and after 30 days on a prescribed low-calcium and normal oxalate diet (11 and 1.1 mmol respectively). Under both conditions, the excretion of the main urinary parameters related to dietary composition, electrolytes, oxalate and daily citrate urinary excretion, were measured. The relative supersaturation of calcium oxalate was calculated by means of an iterative computer method which takes into account the main soluble complex species on which the solubility of calcium oxalate is dependent. In addition, intact parathyroid hormone and 1,25-dihydroxyvitamin D blood levels were also evaluated. In 13 of the patients intestinal calcium absorption was evaluated during both a free- and a low-calcium diet, utilizing kinetics methodology. 4. The low-calcium diet induced, together with an expected reduction of calcium excretion, a marked increase in oxalate urinary output. This finding was independent of the presence or otherwise of hypercalciuria and of the serum levels of parathyroid hormone and vitamin D. Intestinal calcium absorption was also stimulated by calcium deprivation and its levels were well correlated with oxalate excretion. Minor changes in magnesium and citrate excretion were also observed. The overall effect on the relative supersaturation of calcium oxalate consisted in a substantial increase in this parameter during the low-calcium diet. 5. In conclusion, our data reinforce the concept that dietary calcium restriction has potentially deleterious effects on lithogenesis, by increasing the relative supersaturati

Topics: Adult; Calcium; Calcium Oxalate; Calcium, Dietary; Citric Acid; Female; Humans; Hydroxyproline; Intestinal Absorption; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Uric Acid; Urine

Formation of renal stones requires supersaturation (SS) high enough to induce crystallization; such a SS is referred to as the upper limit of metastability (ULM). The ULM for calcium oxalate (CaOx) or calcium phosphate can be measured by adding oxalate or calcium to urine, respectively, and noting the point at which overt crystallization occurs as evidenced by clouding. In principle, the urine should be more prone to form stone crystals as its SS approaches the ULM, and the SS ULM distance has been used as an index of stone forming potential. In addition, one would expect the ULM and initial SS to be unrelated, as the starting urine SS has no apparent link to the amount of calcium or oxalate that urine can dissolve without leading to crystal formation. However, in rats, we have found a surprising correlation between ULM and SS, such that ULM appears to rise with initial SS, for CaOx, and, to a lesser extent, for brushite (Br), a typical calcium phosphate initial phase. In this study, we measured CaOx and Br ULM, and SS, in urine of 50 patients and 11 normal people, to determine if ULM and SS were correlated, as in rats, and to explore the relationship between SS and ULM. We found the same dependence of ULM on SS as in rats, for both CaOx and Br, and found no differences between patients and normal people with respect to this dependency. However, for Br, patients showed a lower ULM than normals, but the same initial SS, meaning that patients were closer to their crystal formation threshold than normals. Treatments for stones had no apparent effect on the SS-ULM dependency. We conclude that in humans, as in rats, ULM is related to initial SS, and that this relationship is the same in patients as in normals for CaOx, but shifted in a stone forming direction for Br among patients. The ULM-SS interaction is unaffected by contemporary conventional stone treatments, and is more marked for CaOx than Br. The mechanisms of the dependence are unknown. The smaller difference between ULM and initial SS for Br in patients than normal supports prior evidence suggesting a defect in stone patients that could lead to calcium phosphate crystallization, subsequent nucleation of CaOx, and stone disease.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Crystallization; Female; Humans; Kidney Calculi; Male; Oxalates; Phosphorus; Solubility; Titrimetry

A kinetic method for the determination of vitamin C, citrate and oxalate in their mixture is described. The method involves the use of cerium(IV) as an oxidant and measurement of reaction rates spectrophotometrically by following the decrease in absorbance of cerium(IV) at 410 nm. The adaptive Kalman filter was used for data manipulation and analysis. It is shown that the use of the Kalman filter is superior to the classical differential kinetic methods owing to its suitability for the determination of analytes that react with a single reagent and exhibit a reaction rate constant ratio of less than 1.5. The results obtained were found to be highly precise and accurate even in the presence of some expected interferents.

Topics: Absorption; Algorithms; Ascorbic Acid; Citrates; Humans; Kidney Calculi; Oxalates

Topics: Administration, Oral; Adult; Female; Humans; Kidney Calculi; Oxalates; Pyridoxine

To evaluate the possible traumatizing effect of high-energy shockwaves (HESW) on new stone formation as indicated by crystal deposition in the renal parenchyma, we performed an experimental study in 50 rabbits. During severe oxaluria induced by continuous ethylene glycol (0.75%) administration, animals in the first group (N = 15) received 500 to 1500 shockwaves. Animals in the second group (N = 15) underwent no specific therapy apart from ethylene glycol administration. In a third group of animals (N = 15), only shockwave administration was applied. Sham group animals constituted the last group in our study (N = 5). Three months after shockwave application, tissue sections obtained from treated and untreated kidneys were evaluated histopathologically under light and transmission electron microscopy (TEM) for the presence and degree of crystal deposition in the cortical parenchymal region subjected to HESW. Crystal deposition was evident in the intercellular region and intratubular parts of the parenchyma in animals subjected to HESW application, especially in those receiving relatively high (1000 or 1500) numbers of shockwaves. On the other hand, no crystal formation and deposition was detectable in animals undergoing only ethylene glycol therapy or shockwave administration alone. Sham group animals demonstrated no significant renal histopathology. The traumatic effects of HESW should be evaluated as a factor in new stone formation after SWL.

Topics: Animals; Crystallization; Disease Models, Animal; Ethylene Glycol; Ethylene Glycols; High-Energy Shock Waves; Kidney; Kidney Calculi; Microscopy, Electron; Oxalates; Prospective Studies; Rabbits; Recurrence

Using ethylene glycol (EG) and vitamin D3 as crystal-inducing diet (CID) in rats, we investigated the effect of the dosage of EG on the generation of chronic calcium oxalate (CaOx) nephrolithiasis. We collected weekly 24 hour urines and measured herein the amount of oxalate, calcium, glycosaminoglycans (GAG's), creatinine, protein, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (gamma-GT), and N-acetyl-beta-glucosaminidase (NAG). The potential of these urines to inhibit crystal growth and agglomeration was also evaluated. After four weeks, the kidneys were screened by histology and radiography for the presence of CaOx crystals and the amount of kidney-associated oxalate was biochemically measured. Using 0.5 vol.% EG, only a part of the rats showed CaOx deposition in the renal cortex and/or medulla, without obvious differences between Wistar and Sprague-Dawley (SD) rats. If a dietary EG concentration of 0.75, 1.0, or 1.5 vol.% was used, the amount of kidney-associated oxalate was proportionally higher and CaOx crystal formation was consistently found in all rats. Most crystals were encountered in the cortex, whereas in the medulla and the papillary region, crystals were only occasionally detected. From these data, we conclude that in the chronic rat model, based on EG and vitamin D3, a consistent deposition of CaOx crystals is obtained using a EG concentration of at least 0.75%.

Topics: Animals; Calcium; Calcium Oxalate; Cholecalciferol; Crystallization; Ethylene Glycol; Glycosaminoglycans; Kidney; Kidney Calculi; Male; Oxalates; Rats; Rats, Sprague-Dawley; Rats, Wistar

We describe a method for measuring urinary oxalate and citrate with capillary electrophoresis (CE) and indirect ultraviolet absorbance detection. Sample preparation is minimal, requiring an acidification, brief centrifugation, and dilution. The method is rapid, with oxalate and citrate having mean migration times of 4.02 and 4.50 min, respectively. The minimal detectable concentration (signal-to-noise ratio of 7) of both oxalate and citrate in urine was 7 mg/L. Total imprecisions (CV) were 1.2-5.6% for three urine samples with oxalate and citrate concentrations of 8-60 mg/L and 80-860 mg/L, respectively. The recovery of added oxalate ranged from 94% to 101%. Results of CE analyses agreed well with enzymatic determinations of oxalate and citrate. Rapid analysis time, accuracy, and reproducibility make this procedure well suited for routine urinary oxalate and citrate determinations.

Topics: Capillary Action; Citrates; Citric Acid; Electrophoresis; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Oxalic Acid; Sensitivity and Specificity

A clinical investigation was carried out on patients with uric acid stones in order to study the frequency and pathogenesis of uric acid nephrolithiasis. Of 652 patients with stones in the upper urinary tract in whom the stone composition could be examined, 36 patients and uric acid stones (5.5%). The male to female ratio was 11:1. The average age of the 33 male subjects was 49 +/- 11 years (mean +/- SD), and the 3 females were 22, 37 and 42 years old, respectively. Two of the females showed hypouricemia. With regard to stone composition, pure uric acid stones were present in 26 cases (72%), a mixed uric acid and calcium oxalate stones were found in 6 cases (17%), both pure uric acid and mixed uric acid and calcium oxalate stones were observed in 3 cases (8%), and a mixed uric acid and sodium acid urate stone in 1 (3%). Biochemical studies on male patients showed that the blood uric acid level was higher in the uric acid stone group and the pure uric acid stone group compared to the calcium stone group. The blood uric acid levels of the former 2 groups did not differ from the control group. With respect to urine chemistry, the excretion of calcium in the uric acid stone group was significantly lower than that in the control group. In the uric acid stone group and the pure uric acid stone group the excretion of calcium tended to be lower than that in the calcium stone group. The amounts of oxalic acid excreted in the uric acid stone group and in the pure uric acid stone group were low compared to the calcium stone group. Oxalic acid elimination in these 2 groups did not differ from the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Age Distribution; Aged; Aluminum; Biomarkers; Calcium Oxalate; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Sex Factors; Uric Acid; Urine

In a paper published in 1974, it was reported that uro-oxalic stones are found more often in subjects with group O than with group A blood types although the proportions of these two blood types are approximately equivalent in the French population. The present work confirms these data, the ratio of group O to group A renal lithiasis being approximately 3 to 1. In a paper published in 1987, uro-oxalic stones were found to occur preferentially on the left side: 84 on the left and 39 on the right. The present work confirms this notion since in 57 cases, stones were bilateral in 2 cases, on the left in 39 and on the right in 16. Extra corporeal shock wave lithotripsy was performed in 40 of the 57 cases and showed that uro-oxalic stones are most resistant to shock-waves than the other types of stones. They are about as hard as calcium oxalate monohydrate stones or harder in certain cases: A mean of 3,865 shock-waves were required in the 40 cases of the uro-oxalic lithiasis treated with the HM3 Dornier device, while the mean number of shock-waves required for all types of stones in general varies from 2,000 to 2,500. In 4 cases, 5,000 or 6,000 high power shock-waves (7,000 in one session and 9,500 in two sessions) had to be used to obtain a satisfactory result. The calcium oxalate part of these stones is almost always composed of calcium oxalate monohydrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Blood Group Antigens; Humans; Kidney Calculi; Lithotripsy; Oxalates; Retrospective Studies; Uric Acid

A preliminary diagnosis of the disease responsible for the stones is essential to allow appropriate medical treatment of renal stones. In this paper, the authors describe their diagnostic and treatment protocol based on computer-assisted urinary metabolic analysis. 413 subjects, divided into four groups, were prospectively evaluated to calculate their specificity, sensitivity, reproducibility and efficacy and to demonstrate the usefulness of this protocol.

Topics: Absorption; Adolescent; Adult; Aged; Calcium; Citrates; Citric Acid; Clinical Protocols; Creatinine; Cystinuria; Diagnosis, Computer-Assisted; Female; Follow-Up Studies; Humans; Hyperoxaluria; Kidney Calculi; Magnesium; Male; Metabolic Diseases; Middle Aged; Oxalates; Oxalic Acid; Prospective Studies; Reproducibility of Results; Sensitivity and Specificity; Uric Acid

Structural analysis of human kidney stones reveals the presence of cellular membranes and other cell fragments. Experimentally, calcium oxalate crystallization is facilitated when an exogenous nephrotoxin is given with ethylene glycol, thus providing cellular degradation products to act as heterogeneous nuclei. In this report, we tested whether oxalate alone could act as a cell toxin capable of producing damaged cells without the presence of an exogenous agent. Cultured LLC-PK1 and MDCK cells, when exposed to 1.0 mmol KOx, a concentration at the limit of metastability for calcium oxalate nucleation, were severely damaged as measured by specific lactate dehydrogenase (LDH) release in the spent media and by trypan blue exclusion. This effect was magnified by the addition of pre-formed calcium oxalate monohydrate crystals; the injury was significantly amplified when compared to exposure to oxalate alone. Scanning electron microscopy studies illustrated attachment of crystals to cells with loss of cell-to-cell and cell-to-substrate contact, as cells were released from the monolayer. In both oxalate and combined crystal-oxalate studies, more cells were released from the monolayer and exhibited considerably more damage when compared to controls. Oxalate, at the limit of metastability for calcium oxalate, is a cell toxin and can produce cellular degradation products. This effect is increased significantly by the addition of calcium oxalate monohydrate crystals.

Topics: Animals; Calcium Oxalate; Cell Line; Cell Survival; Crystallization; Dogs; Humans; Kidney; Kidney Calculi; LLC-PK1 Cells; Microscopy, Electron, Scanning; Models, Biological; Oxalates; Oxalic Acid; Swine

We have recently suggested that vitamin A could protect against experimental lithiasis by repairing tubular membrane cells or protection against membrane damage caused by free radicals generated during experimental lithiasis. Although vitamin E treatment demonstrated no beneficial effect on stone formation, it promoted the repair mechanism by vitamin A during experimental lithiasis and by supported the hypothesis that oxalate crystals may be destructive to renal epithelium because they are large and irregular.

Topics: Animals; Calcium; Cell Membrane; Drug Synergism; Epithelium; Free Radicals; Kidney; Kidney Calculi; Kidney Tubules; Male; Oxalates; Oxalic Acid; Rats; Rats, Wistar; Urea; Vitamin A; Vitamin E

The paper presents the results of clinical and laboratory examination made in 3 groups of children: populational, hospital and control (a total of 176 patients). The children were diagnosed to have variants of dysmetabolic nephropathy (DN) which had become a problem not only for urolithiasis-endemic regions, but also for the Middle Russia. The study involving characterization of cytomembranes, renal tissue biopsy allowed conclusion on nonspecific DN symptoms. Obligatory symptoms were those of OCC, microhematuria and/or mild proteinuria, changes in cytomembranes, weak tubular function, tubulo-interstitial changes. DN genesis is thought multifactorial, involving genetic predisposition, biochemical defects, ecological hazards.

Topics: Adolescent; Biopsy; Child; Child, Preschool; Chronic Disease; Crystallization; Humans; Incidence; Infant; Kidney; Kidney Calculi; Kidney Diseases; Lipids; Moscow; Oxalates; Terminology as Topic

Topics: Acute Disease; Acute Kidney Injury; Adenocarcinoma; Anuria; Ascorbic Acid; Humans; Infusions, Intravenous; Kidney Calculi; Male; Middle Aged; Oxalates; Prostatic Neoplasms

Oxalate lithiasis was induced in control rats and rats previously given a vitamin A supplement for one week at the dose for 200 UI/d/kg body weight. Oxalate and calcium deposits in renal tissue measured 24 hours after the induction of lithiasis were found to be significantly lower in the vitamin A supplemented rats (p < 0.001 and p < 0.01) respectively). Renal function in these animals was also improved as compared with controls (p < 0.05). However, when vitamin A supplements were given for the same period and at the same dose, but after the induction of oxalate lithiasis, no difference regarding oxalate and calcium deposits was found between the two groups of animals. The same applied to renal function, which showed no improvement in the supplemented animals as compared with controls. These results suggest that vitamin A supplements have an inhibitory effect on lithogenesis but probably no litholytic action as such. The effect of vitamin A is probably related to its action on tubular cellular repair or an inhibitory effect on necrosis of these cells.

Topics: Animals; Calcium; Injections, Intramuscular; Kidney; Kidney Calculi; Male; Oxalates; Oxalic Acid; Rats; Rats, Wistar; Urea; Vitamin A

One metabolic pathway for glycine leads to glyoxylate which is the precursor of oxalate. To investigate whether absorption of glycine solution in transurethral operations may promote precipitation of calcium oxalate stones, we collected urine for 24 h before and after an intravenous infusion of 22 g of glycine in 10 male volunteers. There were no significant changes in the urinary excretion of oxalate, calcium, or citrate. Urine volume and amino acid excretion increased, while the urine contained less potassium. These results provide no biochemical evidence of an increased risk of renal lithiasis due to glycine irrigation during transurethral operations.

Topics: Adult; Calcium Oxalate; Glycine; Humans; Kidney Calculi; Kidney Concentrating Ability; Male; Oxalates; Postoperative Complications; Prostatectomy; Risk Factors; Therapeutic Irrigation; Urinalysis

To further evaluate the mechanisms of oxalate (Ox2-) transport in the intestine the following studies were performed using isolated, short-circuited segments of the rabbit distal colon (DC). In control buffer, the DC absorbed Ox2- (net Ox2- flux, JNetOx = 5.4 +/- 0.7 pmol.cm-1.h-1). Replacement of Na+ with N-methyl-D-glucamine (NMDG+) abolished Ox2- absorption by decreasing mucosal to serosal Ox2- flux (JmsOx), without affecting Cl- transport, while gluconate substitution for Cl- did not affect JNetOx or net Na+ flux (JNetNa). Addition of Na+ to the serosal side of tissues bathed by NMDG+ buffer increased JmsOx 40% without altering mucosal to serosal Cl- flux (JmsCl). Serosal amiloride or dimethyl amiloride (10(-3) M) abolished JNetOx by decreasing JmsOx, it increased serosal to muscosal Cl- flux (JsmCl) and it gradually inhibited short-circuit current (Isc). Mucosal amiloride (10(-4) M) abolished Ise but had no effect on Ox2- or Cl- fluxes. Serosal 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 10(-6) M) reduced JmsOx by 20% and JNetOx by 43% without affecting JmsCl or JNetCl. Dibutyryl cyclic adenosine monophosphate (dB-cAMP, 5 x 10(-4) M, both sides) stimulated Ox2- secretion (JNetOx = -12.6 +/- 3.3 pmol.cm-2.h-1). The dB-cAMP-induced secretion of Ox2- and Cl- were fully abolished by serosal furosemide (10(-4) M) and partially inhibited (35%) by 5 x 10(-4) M mucosal NPPB [5-nitro-2-(3-phenylpropylamino)-benzoic acid], a putative Cl- channel blocker.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Animals; Biological Transport, Active; Chlorides; Colon; In Vitro Techniques; Intestinal Absorption; Ion Transport; Kidney Calculi; Male; Meglumine; Models, Biological; Oxalates; Oxalic Acid; Rabbits; Sodium; Sodium-Hydrogen Exchangers

The effect of sodium pentosan polysulphate (SPP) was investigated in calcium oxalate stone forming rats with respect to the urinary excretion of certain risk factors and enzymes. Calcium oxalate stones were induced by feeding 3% w/w sodium glycollate to the rats. Urinary calcium, oxalate, phosphorus and uric acid levels were increased in stone formers. In contrast magnesium excretion was low in this group. SPP treatment lowered oxalate and calcium levels in both controls and experimental animals. Magnesium levels were increased moderately. Increased excretion of urinary enzymes--LDH, alkaline phosphatase, gamma-GT and beta glucuronidase--in calculogenic rats indicates membranuria and damage to proximal tubules during stone formation. Decreased pyrophosphatase activity was observed in glycollate fed rats. SPP treatment decreased the excretion of the above enzymes in the treated groups. Stone formers exhibited decreased LAP and fibrinolytic (urokinase) activities. SPP being associated with fibrinolytic properties, increased the activities of the above two enzymes to that of control levels in calculogenic rats.

Topics: Alkaline Phosphatase; Animals; Calcium; Calcium Oxalate; gamma-Glutamyltransferase; Glucuronidase; Kidney Calculi; L-Lactate Dehydrogenase; Magnesium; Male; Oxalates; Pentosan Sulfuric Polyester; Phosphorus; Rats; Rats, Wistar; Risk Factors; Uric Acid

Urinary excretion of calcium, magnesium, phosphate and oxalate in the condition of low-calcium diet, and the secretion of LH, FSH, testosterone and estradiol following LH-RH stimulation test have been determined in 26 men with active nephrolithiasis and in 14 healthy male subjects. Significantly higher urinary excretion of calcium and oxalate, and significantly lower excretion of magnesium was observed in men with nephrolithiasis as compared to healthy men. In addition, the patients with nephrolithiasis had significantly higher concentrations of testosterone, estradiol and FSH than the healthy controls. The results obtained suggest the participation of the gonadal hormones in the pathogenesis of active nephrolithiasis.

Topics: Adult; Calcium; Estradiol; Gonadotropins, Pituitary; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Testosterone

Topics: Adult; Calcium; Calcium, Dietary; Dairy Products; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates

We determined total blood protein (TBP) and total urine protein (TUP) in healthy subjects and urolithiasis (UL) patients with renal calculi of different chemical composition: phosphate (CaP), oxalate (CaOx) and urate (HUr). We discussed the peculiarities of TBP and TUP distribution curves obtained and showed that the data on TBP and TUP do not make it possible to reliably single out patients with UL or determine the chemical composition of calculi in their kidneys. However, it was established that the comparison of TUP measurement results for UL patients using the Ponseau-S and sulfosalicylic acid methods makes it possible to reliably separate patients with Ca-containing calculi (CaP and CaOx) from those with HUr calculi. The explanation to this phenomenon using the data on the fractional composition of TUP and the organic matrix of those patients' calculi is given.

Topics: Azo Compounds; Benzenesulfonates; Blood Proteins; Coloring Agents; Humans; Kidney Calculi; Oxalates; Phosphates; Proteinuria; Salicylates; Solvents; Uric Acid

A scheme for the chemical microanalysis of renal stone fragments recovered from urine voided immediately after lithotripsy has been developed and evaluated. The analytical procedure includes assay of calcium, magnesium, phosphate, oxalate and urate and has been applied to 78 such urine samples. Problems relating to co-existing crystalluria and blood and urine contaminants have been recognised and overcome. However, significant loss of all stone components due to fragment dissolution in urine prior to recovery was found to occur and was investigated. The distribution of stone components found in these analyses was similar to that seen in previous surveys of intact stones.

Topics: Calcium; Humans; Kidney Calculi; Lithotripsy; Magnesium; Oxalates; Oxalic Acid; Phosphates; Solubility; Uric Acid

In this paper a thorough study on the composition and structure of calcium oxalate monohydrate (COM) papillary calculi is presented. In 86.4% of these calculi, small amounts of phosphates were detected and generally located at the calculi core. This demonstrates the importance of phosphates as the heterogeneous nucleus of 'pure' COM calculi. Study of the main biochemical parameters of these patients showed that the most frequent biochemical alteration was associated with hypocitraturia (25%), whereas hypercalciuria and/or hyperoxaluria were detected in very few cases. With respect to the urinary pH values, 70% of the patients presented values lower than 6 and 30% higher than 6. These facts indicate that in a number of cases the formation of phosphates is not the result of persistent high urinary pH values, and the presence of occasional papillary microinfections must be suspected. It is clear that, by avoiding the formation of heterogeneous phosphate nuclei, 'pure' COM calculi would not develop, and consequently therapies for these individuals under these conditions must take this into account.

Topics: Calcium; Calcium Oxalate; Citrates; Humans; Kidney Calculi; Microscopy, Electron, Scanning; Oxalates; Phosphates; Spectrophotometry, Infrared

Hypercalciuria and nephrocalcinosis are not uncommon in patients with Wilson's disease but have only once been reported as the presenting sign. We diagnosed Wilson's disease in a 17-year-old male patient 6 years after his first episode of gross hematuria and 2 years after detection of hypercalciuria and nephrocalcinosis. Therapy with penicillamine resulted only in a moderate reduction of urinary calcium excretion but oxalate excretion increased.

Topics: Adolescent; Calcium; Hematuria; Hepatolenticular Degeneration; Humans; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Oxalic Acid; Penicillamine; Time Factors; Ultrasonography

To study the structural composition of 61 renal and 9 vesical large lamellated non-infection urinary tract stones, samples from successive layers were quantitatively analyzed with standard chemical techniques, but with a new classification based on percentage composition of ions rather than compounds. The commonest pattern of composition (n = 41) was that of the lamellar stones of one stone type (uric acid, oxalate, or phosphate) and group (according to % of indicating ion), followed by bilamellar stones of different stone types (17) or of one stone type but different groups (8). The other stones were trilamellar (3) or quadrilamellar (1) of different stone types. In the 29 stones with lamellae of different type and/or group, the chemical composition of successive layers seemed to confirm the correlation between uric acid and oxalate, rather than phosphate, ions and between oxalate and both uric acid and phosphate ions. An influence on these correlations either positive or negative, may be the responsible factor for specifying the type and group of a forming stone or layer of a stone. The observed ionic correlations within the stones seem to support the choice of the oxalate ion, in the uric acid or phosphate stones, and both of the uric acid and phosphate ions, in the oxalate stones, as indicating ions for grouping in our proposed classification of urinary stones.

Topics: Humans; Kidney Calculi; Oxalates; Phosphates; Uric Acid; Urinary Bladder Calculi

The effect of the calcium antagonist verapamil on urinary calcium and oxalate excretion was examined and compared with that of trichlormethiazide to evaluate whether verapamil is useful in the prevention of calcium oxalate renal stones. Twenty-four-hour urine of 16 renal stone formers was measured at the outpatient clinic before and after administration of 120 mg/day verapamil for a mean duration of 2.7 months (range, 2 weeks to 6 months). The 24-hour urine was analyzed for creatinine, calcium, oxalic acid, magnesium and citric acid and the results compared with those in 20 renal stone formers who were administered trichlormethiazide. Verapamil was found to significantly reduce the urinary oxalate excretion of the 5 hyperoxaluric (> or = 50 mg/day) patients but no significant effect on urinary calcium, magnesium or citric acid was observed. Conversely, trichlormethiazide significantly decreased urinary calcium excretion in the hypercalciuric (> or = 250 mg/day) patients. Calcium oxalate risk index of hypercalciuric and hyperoxaluric patients was significantly reduced after the administration of verapamil. These findings suggest that verapamil is effective in reducing urinary oxalate excretion in the hyperoxaluric patients.

Topics: Calcium; Citrates; Citric Acid; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Trichlormethiazide; Verapamil

19 patients with active nephrolithiasis, 14 patients with non-active nephrolithiasis and 17 healthy subjects were examined. After 7 days consumption of standardized low calcium, low phosphate, low purine and low protein diet, plasma parathyroid hormone (PTH) and osteocalcin concentration, activity of the alkaline phosphatase and its bone fraction were assessed before and after 4 hours i.v. infusion of calcium gluconate (15 mg/kg b.w. in 500 ml 0.9% NaCl). In addition, urinary excretion of oxalate, calcium, phosphate and magnesium were estimated in all examined groups.. 1. In comparison to healthy subjects, patients with nephrolithiasis are characterized by higher plasma PTH and osteocalcin concentration, increased activity of bone fraction of alkaline phosphatase and urinary oxalate and calcium excretion. 2. Disturbances of calcium-phosphate and oxalate metabolism, PTH secretion and bone osteoblastic activity found in patients with active nephrolithiasis are qualitatively similar but quantitatively more intensive than in patients with non-active nephrolithiasis.

Topics: Adult; Alkaline Phosphatase; Biomarkers; Bone and Bones; Calcium; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Reference Values

1. Vitamin D seems to play an essential role in the pathogenesis of idiopathic hypercalciuria at least in part via intestinal hyperabsorption of calcium. Hyperabsorption of calcium, in turn, might enhance the intestinal uptake of free oxalate, thus leading to hyperoxaluria. To verify this hypothesis we studied 75 calcium-stone-formers subdivided as follows: group 1 (15 patients) with isolated hyperoxaluria; group 2 (25 patients) with hyperoxaluria and hypercalciuria; group 3 (22 patients) with isolated hypercalciuria; group 4 (12 patients) with no metabolic abnormalities. 2. As expected, urinary calcium excretion differed in the various groups (P < 0.001), being highest in groups 2 and 3; urinary oxalate excretion, by definition highest in groups 1 and 2, was even more pronounced in group 2 than in group 1 (P < 0.05). Although in the normal range, the serum 1,25-dihydroxyvitamin D concentration was higher (P < 0.001) in the two hypercalciuric groups (2 and 3), showing peak levels in group 2. 3. When the data from the 75 stone-formers were pooled, there was a positive correlation between the serum concentration of 1,25-dihydroxyvitamin D and urinary calcium excretion (P < 0.001) and urinary oxalate excretion (P < 0.003), the latter relationship also being present when only the two hypercalciuric groups (groups 2 and 3) were considered together (P < 0.05). 4. Our data seem to confirm a relevant role for the vitamin D system in the pathogenesis of calcium nephrolithiasis due to increased intestinal calcium absorption, but also because this in turn induces a greater intestinal absorption of oxalate, thus leading to the occurrence or exacerbation of hyperoxaluria.

Topics: Adult; Aged; Calcitriol; Calcium; Female; Humans; Hyperoxaluria; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Vitamin D

This study was carried out to verify the hypothesis of a link between faster endogenous phosphorylation of band 3 protein, the anion carrier, and anomalous oxalate transmembrane self-exchange found in erythrocyte from calcium oxalate renal stone formers. Agents able to modify 32P-labelling of band 3 protein induced a concurrent modification in oxalate transmembrane flux. Cyclic AMP- and phospholipid-sensitive Ca(2+)-independent protein kinases seem to be critical modulators of band 3 function. These observations demonstrate a close link between the band 3 phosphorylation state and its anion transport function, and provide new insights into the pathogenetic mechanisms of the cellular anomalies observed in calcium-oxalate renal stone disease.

Topics: Anion Exchange Protein 1, Erythrocyte; Anions; Biological Transport; Calcium Oxalate; Cyclic AMP; Erythrocyte Membrane; Humans; Kidney Calculi; Oxalates; Oxalic Acid; Phosphorus Radioisotopes; Phosphorylation

Topics: Adult; Calcium Oxalate; Calcium, Dietary; Diet; Female; Humans; Kidney Calculi; Male; Oxalates; Prospective Studies

Topics: Calcium Oxalate; Erythrocyte Membrane; Humans; Kidney Calculi; Oxalates

A retrospective analysis of oxalate status in 115 stone-forming individuals revealed hyperoxaluria in 30%. These individuals could be divided into two distinct groups according to urinary oxalate excretion patterns and plasma oxalate levels. The cause of hyperoxaluria in one group may be explained on the basis of increased absorption of dietary oxalate and decreased renal clearance. Hyperoxaluria in the other group appears to be a consequence solely of enhanced endogenous production of oxalate. These two entities can be distinguished from one another in the context of a routine metabolic evaluation of calcium stone disease when urine and plasma oxalate measurements are included.

Topics: Adult; Aged; Biological Transport, Active; Female; Humans; Hyperoxaluria; Kidney; Kidney Calculi; Male; Middle Aged; Oxalates; Risk Factors

The influence of sodium pentosan polysulphate was studied on the deposition of stone forming constituents along with certain enzymes in the renal tissue of experimentally induced urolithiatic rats. Calcium, oxalate and phosphorus levels were elevated in kidneys of lithogenic rats, while SPP administration reduced these levels to near control values. The elevation in kidney LDH was significant in the stone forming groups and SPP had minimal effect. Increases in the activities of Na+, K(+)-and Ca(2+)-ATPases in the calculogenic groups was lowered considerably with SPP treatment. Inorganic pyrophosphatase activity was reduced significantly in the calculogenic as well as in the drug treated groups. Leucine aminopeptidase was decreased in the calculogenic group. SPP treatment elevated the enzyme activity in the treated groups. Reduction in kidney oxalate with SPP may prove useful in the medical management of urolithiasis.

Topics: Animals; Calcium; Kidney; Kidney Calculi; Magnesium; Male; Oxalates; Pentosan Sulfuric Polyester; Phosphorus; Rats; Rats, Inbred Strains

Whether pyridoxine (B6) supplements decrease plasma oxalate concentrations in patients on maintenance dialysis is unresolved. The effect of two dose levels of B6, 0.59 mmol/day (100 mg/day) over 6 months and 4.43 mmol (750 mg) after each dialysis treatment for 4 wk, on plasma oxalate and oxalate removal rate (dialysis plus urinary excretion) was studied in patients on maintenance hemodialysis. In both studies, a control group unsupplemented with B6, who remained on their regular diet, was also studied. The vitamin B6 status of the patients was assessed by the erythrocyte glutamate pyruvate transaminase activity and index before and during supplementation. No decrease in plasma oxalate or oxalate removal rate was found in either study. The plasma oxalate and oxalate removal rates of the unsupplemented hemodialysis patients were not different from those receiving B6 either before or after supplementation. These studies demonstrate that high-dose B6 supplementation does not decrease plasma oxalate concentration in a population of hemodialysis patients.

Topics: Alanine Transaminase; Creatinine; Humans; Hyperoxaluria; Kidney Calculi; Kidney Failure, Chronic; Oxalates; Pyridoxine; Renal Dialysis; Uremia; Vitamin B 6 Deficiency

Oxalate-containing kidney stones are the most common type (75%) of renal stones. In order to control oxalate excretion in the urine, a basic understanding of the cellular transport of oxalate is imperative. We have utilized the technique of continuous cell culture to establish and characterize a model system to study renal epithelial cell (LLCPK1) oxalate transport. Our data demonstrate that oxalate uptake in these cells is dependent on time, concentration and energy. The Km for oxalate uptake was 200 microM. Oxalate uptake was decreased at lower temperatures and elevated in an acidic extracellular environment. Both anion exchange inhibitors DIDS and SITS inhibited oxalate uptake. Sulfate, chloride, and bicarbonate decreased oxalate uptake, as did the diuretics bumetanide and furosemide. There was no evidence for the co-transport of oxalate with sodium. Our data show that monolayers of cultured kidney epithelial cells are a valuable model system for study of the basic cellular mechanisms of oxalate transport.

Topics: Animals; Biological Transport; Cell Line; Epithelial Cells; In Vitro Techniques; Kidney; Kidney Calculi; Oxalates; Swine

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.

Topics: Adult; Biomarkers; Calcium; Calcium Oxalate; Citrates; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Prognosis; Recurrence; Risk Factors; Uric Acid

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.

Topics: Adult; Aged; Calcium; Calcium, Dietary; Citrates; Citric Acid; Creatinine; Drug Combinations; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Oxalic Acid; Phosphorus

The effect of fluorine (F) on stone formation induced by ethylene glycol (EG) was studied in rats. For different groups, the drinking water was supplemented with EG, sodium fluoride (NaF), EG+NaF, or nothing as control. An isotope-tracing method was used to evaluate experimental stone formation in the kidneys by introducing 45Ca intraperitoneally into rats and then measuring the radioactivity of the kidney. At the end of the 4-week experiment, rats of the EG+NaF group showed a significantly lower incidence of gross urinary stones and lower 45Ca activity in their kidneys compared to the EG group of rats. Both the EG group and EG+NaF group had markedly increased urinary oxalate excretion, with the latter significantly lower than the former (p less than 0.05). Urinary oxalate excretion was relatively lower in the NaF group than in the control group. This study indicates that NaF can inhibit renal stone formation induced by EG by decreasing oxalate synthesis and urinary oxalate excretion, and suggests a possible clinical therapeutic value of NaF in the prevention of oxalate kidney stones.

Topics: Animals; Calcium Radioisotopes; Ethylene Glycol; Ethylene Glycols; Kidney; Kidney Calculi; Male; Oxalates; Radionuclide Imaging; Rats; Rats, Inbred Strains; Sodium Fluoride

Recently a technique to measure intact parathyroid hormone (PTH), i.e. the biologically active hormone, has been available. The aim of the present study was to apply this method to evaluate the parathyroid function in a material of recurrent renal stone formers (n = 324). Intact PTH was found to be inversely related to both urinary calcium (r = -0.15; p less than 0.01) and serum calcium (p less than 0.02) indicating that in the majority of the patients with hypercalciuria this was accounted for by intestinal hyperabsorption and not by high serum PTH. Hyperabsorption was also the likely explanation for the finding of a positive relationship between the urinary calcium and oxalate excretions (r = 0.22; p less than 0.001) in medication-free patients without intestinal disorders, i.e. without enteric hyperoxaluria. Altogether 25 patients (7%) had elevated serum PTH concentrations. They were followed up with fasting serum and urinary electrolytes and an oral calcium loading test (1 g of calcium) in order to evaluate the importance of renal and intestinal factors responsible for the elevated serum PTH concentrations. The investigation was carried out on a free diet and on low and high calcium intakes, respectively. The incidence of intestinal malfunction, which was sometimes present without clinical symptoms, was found to be approximately the same as that of impaired renal conservation of calcium. The findings in the patients with intestinal malfunction were a reduced intestinal absorption of calcium and an enhanced tubular reabsorption of calcium (TRCa), with greater reabsorption of calcium for higher PTH values. In patients with impaired renal conservation of calcium despite the raised PTH there was no correlation between PTH and TRCa. When PTH was suppressed during the oral calcium load the TRCa was found to be inappropriately low and the renal defect obvious. The intestinal calcium absorption was secondarily increased to compensate for the renal losses.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Calcium; Female; Humans; Intestinal Mucosa; Kidney Calculi; Kidney Tubules; Male; Middle Aged; Oxalates; Parathyroid Glands; Parathyroid Hormone

Single intraperitoneal injections of three, seven, or 10 mg. of sodium oxalate per 100 gm. of rat body weight were administered to male Sprague-Dawley rats. At various times after the injection, urine samples were analyzed for oxalate, and urinary enzymes, alkaline phosphatase, leucine aminopeptidase, gamma-glutamyl transpeptidase, and N-acetyl-beta-glucosaminidase. The kidneys were processed for light microscopy and renal calcium and oxalate determination. Oxalate administration resulted in an increase in urinary oxalate and formation of calcium oxalate crystals in the kidneys. The amount and duration of urinary excretion of excess oxalate and retention of crystals in the kidneys correlated with the dose of sodium oxalate administered. At a low oxalate dose of three mg./100 gm., crystals moved rapidly down the nephron and cleared the kidneys. At higher doses crystals were retained in kidneys and at a dose of 10 mg./100 gm. were still there seven days post-injection. Crystal retention was associated with enhanced excretion of urinary enzymes indicating renal tubular epithelial injury.

Topics: Acute Disease; Animals; Calcium; Calcium Oxalate; Histocytochemistry; Hyperoxaluria; Kidney; Kidney Calculi; Male; Oxalates; Rats; Rats, Inbred Strains

Administration of ascorbic acid, at 150 mg/100 ml of water intake, for one month, induced hyperoxaluria in the rats (P less than 0.001) and decreased citraturia (P less than 0.001) magnesuria (P less than 0.001) and pyrophosphaturia (P less than 0.01). The same disorders were observed when the dose administered was 300 mg/100 ml, excepted that oxaluria was considerably enhanced in this group. Despite these variations, renal deposits were not observed, even in the animals receiving 300 mg of ascorbate/100 ml of water intake. This protection was due to decreased calcium excretion (P less than 0.01 in two groups) and probably to acidification of the urine.

Topics: Animals; Ascorbic Acid; Calcium; Citrates; Citric Acid; Diphosphates; Drug Evaluation, Preclinical; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains

Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation. There is evidence that glycosaminoglycans (GAGs) have a regulatory effect on both of these processes. This study tested the hypothesis that modifications of erythrocyte oxalate self-exchange induced by oral GAGs are paralleled by similar changes in overall oxalate metabolism. 40 patients with idiopathic calcium-oxalate nephrolithiasis were treated for 15 days with 60 mg/day of a mixture of GAGs. By day 15 of treatment there were significant reductions from baseline in erythrocyte oxalate self-exchange (mean [SD] 1.67 [1.18] vs 2.59 [1.63] x 10(2) per min; p less than 0.005) and erythrocyte membrane protein phosphorylation (55.8 [7.3] vs 72.9 [6.8] x 10(-3) cpm/mg protein; p less than 0.005), but also in urinary oxalate excretion (0.24 [0.09] vs 0.31 [0.15] mmol/24 h; p less than 0.005). This finding suggests similar changes in both erythrocytes and other cells more important in oxalate handling. The changes had reversed by 15 days after withdrawal of treatment. Acute intravenous administration of GAGs (60 mg) induced a fall in carbon-14-labelled oxalate renal clearance (143 [13] vs 169 [28] ml/min; p less than 0.005), which strongly suggests the participation of the kidney. However, reduced oxalate absorption from the intestine, and even decreased synthesis of oxalate, cannot be ruled out.

Topics: Administration, Oral; Adult; Analysis of Variance; Biological Transport; Calcium Oxalate; Erythrocytes; Female; Glycosaminoglycans; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid

The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.

Topics: Animals; Calcium; Copper; Dietary Carbohydrates; Energy Intake; Kidney; Kidney Calculi; Magnesium; Male; Organ Size; Oxalates; Phosphorus; Rats; Rats, Inbred Strains; Risk Factors; Sucrose; Zinc

The presence of mild hyperoxaluria in recurrent calcium oxalate stone formers is controversial. The aim of this study was to identify recurrent stone formers with mild hyperoxaluria and to classify them further by assessing their response to a low oxalate diet. In addition, the prevalence of other risk factors for stone formation in this group of patients was investigated. A total of 207 consecutive patients with recurrent renal calculi were screened and 40 (19%) were found to have mild hyperoxaluria. Of these, 18 (45%) responded to dietary oxalate restriction by normalising their urinary oxalate. The remaining 22 patients were classified as having idiopathic hyperoxaluria and were subdivided into those in whom urinary oxalate excretion was consistently elevated in all specimens measured and those in whom the elevation was intermittent in nature. Dietary oxalate restriction had a partially beneficial effect in lowering oxalate excretion in the patients with persistent hyperoxaluria. No difference in urinary oxalate excretion was found after dietary restriction in the patients with intermittent hyperoxaluria. Other risk factors, including dietary, absorptive and renal hypercalciuria and hypocitraturia, were documented, the prevalence of which (65%) was not significantly different from that (62.5%) found in 40 age- and sex-matched calcium stone formers without hyperoxaluria. The prevalence of hyperuricosuria was significantly greater in patients with hyperoxaluria when compared with stone controls. Further studies are required to elucidate the underlying mechanisms of hyperoxaluria in recurrent stone formers.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Diabetes Complications; Diet; Humans; Hyperoxaluria; Kidney Calculi; Oxalates; Recurrence; Risk Factors

Oxalate transports on membranes of red blood cell, intestinal epithelium and proximal tubule cell were reviewed, and the new findings about oxalate transport across these membranes are reported. Red blood cell oxalate influx rate in a group of recurrent calcium oxalate stone formers was significantly higher than that of a control group. In the red blood cells of mammals, the band 3 protein transports oxalate. Although abnormal influx rate of red blood cells might be recognized as an expression of somatic cell abnormality of oxalate transport in some recurrent stone formers, the band 3 protein is not related to oxalate transport in both kidney and intestine. The study using brush border membrane vesicles suggested the presence of Na-oxalate co-transport. In humans, sodium intake increased the oxalate/creatinine ratio of urine. This indicated that excessive sodium intake might be a risk factor of stone formation. Further study of oxalate transport of both kidney and intestine will be required to elucidate an etiology of calcium oxalate nephrolithiasis.

Topics: Animals; Biological Transport; Calcium Oxalate; Cell Membrane; Epithelium; Erythrocyte Membrane; Humans; Intestinal Mucosa; Kidney Calculi; Kidney Tubules, Proximal; Microvilli; Oxalates; Rats; Rats, Inbred Strains

Sodium oxalate injected into young rats, via the intraperitoneal route, at a dose of 8 mg per 100 g of body weight, induced death in 50 p. cent of animals, and induced calcium oxalate crystals in renal tissue. When a zinc solution was administered prior to sodium oxalate, at the dose of 12 micrograms/100 g of body weight, the mortality rate decreased, and at the same time oxalate and calcium deposits were significant reduced (respectively P less than 0.01; P less than 0.01). The same results were found when zinc was administered at 24 micrograms/100 g of body weight, however, oxalic accumulation was found to be significantly lower in this group than in the group treated at 12 micrograms. This protection against calcium oxalate deposits was complete in the animals treated with various doses of zinc, because compared to reference animals, which received distilled water, calcium accumulation in these groups was not different and oxalate accumulation was also found to be lower (respectively P less than 0.05; P less than 0.001). Microscopic examination showed calcium crystals only in the group treated with sodium oxalate, localized preferentially in the renal papilla. All these experiments conclude on the total inhibitory effect of zinc on experimental lithiasis induced by oxalic acid, even though it was administered at a dose of only 12 micrograms/100 g of body weight.

Topics: Animals; Calcium; Disease Models, Animal; Drug Evaluation, Preclinical; Kidney Calculi; Male; Oxalates; Rats; Rats, Inbred Strains; Sulfates; Zinc; Zinc Sulfate

Intraperitoneal injection of sodium oxalate, at the dose of 8 mg/100 g of body weight, induced into rats oxalate and calcium deposits in renal tissue, compared to animals which received distilled water (respectively P less than 0.05; P less than 0.05). However, when a zinc solution was administered previously, at the dose of 24 micrograms/100 g of body weight, oxalate and calcium accumulation was found to be significantly lower than in the group treated exclusively with sodium oxalate. Similar results were found when the metal used was copper, but oxalate accumulation was found to be significantly higher in this group than in the group treated with zinc (P less than 0.01). Compared to reference animals, which received distilled water, oxalate accumulation was found to be significantly decreased in the groups treated with both zinc (P less than 0.001) and copper (P less than 0.01), whereas calcium accumulation was found to be similar. Microscopic examination showed calcium crystals only in the group treated with sodium oxalate, preferentially localized in the renal papilla. These results suggest that zinc and copper, when administered at the dose of 24 mu/100 g of body weight, completely protect against experimental lithiasis induced by oxalic acid. However, the inhibitory effect of zinc was more pronounced than that of copper, especially against oxalate accumulation.

Topics: Animals; Calcium; Copper; Copper Sulfate; Drug Evaluation, Preclinical; Kidney Calculi; Male; Oxalates; Rats; Rats, Inbred Strains; Sulfates; Zinc; Zinc Sulfate

Topics: Angiography; Female; Humans; Kidney Calculi; Middle Aged; Oxalates; Radioisotope Renography; Uric Acid

Two case histories of patients with end-stage renal disease subsequently found to have primary hyperoxaluria are reported. In the setting of renal failure, the diagnosis is both difficult, due to diminished oxalate excretion, and important, because of frequent graft loss due to oxalate deposition after renal transplantation. The diagnosis was obtained by renal and bone biopsies. Plasma oxalate levels were normal in one patient and the other patient presented with extensive cystic bone lesions. Primary hyperoxaluria should be considered whenever nephrocalcinosis and/or nephrolithiasis are associated with end-stage renal disease.

Topics: Adult; Biopsy; Bone and Bones; Female; Humans; Hyperoxaluria, Primary; Kidney; Kidney Calculi; Kidney Failure, Chronic; Kidney Transplantation; Male; Nephrocalcinosis; Oxalates

Topics: Adult; Female; Humans; Hyperoxaluria; Infant; Interprofessional Relations; Kidney; Kidney Calculi; Male; Nephrology; Oxalates; Pediatrics; Pregnancy; Pregnancy Complications

Following simultaneous liver-kidney transplantation for primary hyperoxaluria type I, although the missing enzyme is provided by the liver transplant, there is a risk of recurrent calcium oxalate crystal formation in the implanted kidney. The necessary kidney protection methods are extrarenal blood purification, principally haemodialysis and haemofiltration, and an abundant diuresis ensured by copious fluid intakes together with prescription of diuretics. These therapeutic measures reduce the oxalate concentrations in both blood and urine. Oxalates are excreted in large amounts over a long period, owing to the formation of important tissue deposits during systemic oxalosis.

Topics: Follow-Up Studies; Hemofiltration; Humans; Hyperoxaluria, Primary; Kidney Calculi; Kidney Transplantation; Liver Transplantation; Oxalates; Recurrence; Renal Dialysis

Eighty stone-forming patients were evaluated as outpatients for risk factors involved in stone formation. Analyses of the major stone risk parameters in the 24-hour collections indicated low volume (less than 2L) in about 79% of these patients. Forty percent of all patients were found to be hypocitraturic, 30% were hyperoxaluric, 18% were hypercalciuric, and 13% were hyperuricosuric. Sixty-one percent of the patients had a normal calcium load study; of these, four patients were uric acid stone formers. The remaining 39% of patients were classified as either absorptive hypercalciuric (16 patients), or fasting hypercalciuric with normal (12 patients) or elevated (3 patients) serum parathyroid hormone (PTH) levels. Of these 31 patients, 61% were not hypercalciuric on the basis of the 24-hour urine collections. The protocol provided a diagnosis in over 98% of patients. Low urinary volume was the only defect found in 5% of patients, while more than one risk factor was identified in 93%.

Topics: Adult; Aged; Calcium; Citrates; Female; Humans; Kidney Calculi; Kidney Function Tests; Male; Middle Aged; Oxalates; Oxalic Acid; Risk Factors; Uric Acid; Urodynamics

Topics: Adult; Biological Transport; Calcium Oxalate; Humans; Hyperparathyroidism; Kidney Calculi; Male; Oxalates; Oxalic Acid; Parathyroidectomy

Topics: Biological Availability; Food; Humans; Kidney Calculi; Oxalates

To better understand the pathogenesis of nephrolithiasis, we developed a new animal model that closely mimics human calcium oxalate stone disease. Rats were treated with a regimen that combines moderate hyperoxaluria (produced by 10 days of feeding with 3% ammonium oxalate) with mild proximal tubular injury/dysfunction (produced by 8 daily injections of gentamicin sulfate -40 mg./kg.). This combined treatment caused a marked increase in the incidence of calcium oxalate crystals and stones over that seen in animals treated with oxalate or gentamicin alone. Using a semiquantitative scoring system for estimating the abundance of crystals in coronal sections of kidneys, we found that 63% of animals receiving gentamicin plus oxalate showed "moderate" numbers of crystal, as compared to 8% of animals receiving oxalate alone; and the majority of the crystals occurred in the papilla, a pattern similar to that seen in human stone disease. Untreated rats and rats treated with gentamicin alone did not exhibit calcium oxalate crystals or stones. Despite the abundance of crystals and stones, animals receiving gentamicin plus oxalate retained relatively normal renal function as judged by creatinine clearance. Thus, the model has several advantages over preexisting models of nephrolithiasis. Crystal and stone deposition develop rapidly (within 14 days). The pattern of deposition resembles that seen in human stone disease and renal function remains relatively normal. These findings indicate that this model of nephrolithiasis may prove useful for studies of the pathogenesis of stone disease. Moreover, they suggest that renal tubular injury and/or dysfunction may produce conditions conducive to the formation and growth of calcium oxalate stones.

Topics: Animals; Calcium Oxalate; Disease Models, Animal; Gentamicins; Kidney; Kidney Calculi; Kidney Tubules; Male; Microscopy, Electron; Microscopy, Electron, Scanning; Oxalates; Rats; Rats, Inbred Strains

To investigate the cellular mechanism(s) underlying kidney stone disease, we examined oxalate uptake in suspensions of renal cortical and papillary cells derived from control and stone-forming animals. In control animals, both cortical and papillary cells exhibited a time-dependent accumulation of oxalate. This uptake was mediated both by passive diffusion and by one or more transport processes sensitive to the anion transport inhibitor, DIDS. Oxalate uptake was also markedly sensitive to extracellular pH, showing increased uptake at acidic pH outside (pHo) (6.0), and reduced uptake at alkaline pHo (8.0). In renal tubular cells from stone-forming animals, oxalate uptake was markedly altered. Uptake was significantly reduced in cortical cells, whereas it was significantly stimulated in papillary cells from the same animals. Since the observed changes in oxalate handling occurred only in stone-forming animals, it is possible that alterations in renal cell oxalate transport contribute to calcium oxalate stone formation.

Topics: 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Animals; Biological Transport; Hydrogen-Ion Concentration; In Vitro Techniques; Kidney Calculi; Kidney Cortex; Kidney Medulla; Kidney Tubules; Male; Oxalates; Rats; Rats, Inbred Strains

Hydrochlorothiazide is employed to reduce calcium excretion in patients with urinary stone disease secondary to renal leak hypercalciuria. Because the drug also has been reported to be a competitive inhibitor of oxalate excretion by the renal tubules, we sought to determine whether chronic use indeed affected the amount of oxalate excreted. Patients taking hydrochlorothiazide 50 mg daily did not have a statistically significant reduction in twenty-four-hour urinary oxalate on their customary diets (pretreatment 37 +/- 3 mg/day [mean +/- S.E.M.; N = 22]; at one year 36 +/- 3 mg/day [N = 22]; at two years 37 +/- 3 mg/day [N = 16]). In 12 patients who voluntarily collected twelve-hour urine specimens after dinner on the third day of a low-oxalate diet and again the next day after a 1 g oxalate load, hydrochlorothiazide had no significant effect on oxalate excretion (19 +/- 2.3 mmol oxalate/mol creatinine on hydrochlorothiazide versus 20.6 +/- 2.6 mmol off the drug after low oxalate meal; 50 +/- 7.8 mmol/mol creatinine on hydrochlorothiazide versus 56.2 +/- 7.5 mmol off the drug after an oxalate load). As expected, there was a significant reduction in urinary calcium excretion and thus of calcium oxalate urinary saturation during hydrochlorothiazide administration. Hydrochlorothiazide by itself is not sufficient to reduce oxalate excretion in patients with renal leak hypercalciuria.

Topics: Adult; Aged; Calcium; Calcium Oxalate; Diet; Female; Follow-Up Studies; Humans; Hydrochlorothiazide; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid

The daily intake of 103 recurrent idiopathic calcium stone formers and 146 controls was assessed by means of a computer-assisted 24-h dietary record. Timed 24-h urine samples were collected over the same period to assess the relationship between dietary intake of nutrients and urinary risk factors for calcium stones. After standardisation for sex, age and social status a total of 128 subjects underwent final statistical analysis; 64 renal stone formers and 64 controls. Significant increases in the consumption of animal and vegetable protein and purine were identified as the nutritional factors that distinguished renal stone formers from controls. As expected, the daily urinary excretion of calcium and oxalate was higher and the daily urinary excretion of citrate was lower in stone formers than in controls. No difference with respect to daily urinary uric acid excretion was recorded. Daily urinary excretion of calcium was correlated to dietary protein intake while daily urinary oxalate was correlated to dietary vitamin C intake. It was concluded that renal stone formers could be predisposed to stones because of their dietary patterns. A link between the protein content of the diet and urinary calcium was confirmed, but dietary animal protein had a minimal effect on oxalate excretion.

Topics: Adult; Aged; Ascorbic Acid; Calcium; Diet; Dietary Proteins; Female; Humans; Kidney Calculi; Male; Middle Aged; Nitrogen; Oxalates; Risk Factors; Socioeconomic Factors

The low incidence of atherosclerosis and other degenerative diseases including stone disease in the Greenland Eskimo has been attributed to their high consumption of oily fish with its high concentration of eicosapentaenoic acid (EPA). Man cannot synthesis EPA from the precursor essential fatty acid, linolenic acid, and can only assimilate preformed EPA present in fish and fish oil, to bring about a change in the pathway of eicosanoid metabolism from the n-6 to the n-3 series. With a westernised diet the oxygenated products of renal prostaglandin synthesis are metabolites of the n-6 series and these are known to play an important role in several pathophysiological states including stone disease. Our previous studies have shown a relationship between prostaglandin activity and urinary calcium excretion and it would seem that the initiating factor/s for stone formation trigger the mechanisms for prostaglandin synthesis resulting in the biochemical abnormalities associated with stone disease. The Eskimo may be protected from these events by possession of an eicosanoid metabolism that follows an n-3 pathway. To test this hypothesis experiments were performed using an animal model of nephrocalcinosis. The animals were divided into three groups; one group was given an intra-peritoneal injection of 10% calcium gluconate daily for 10 days to induce nephrocalcinosis; a second group was fed MaxEPA fish oil before and during the calcium gluconate injections and a third group only received an intra-peritoneal injection of N saline. A group of 12 recurrent, hypercalciuric/hyperoxaluric stone-formers were treated with fish oil for eight weeks to study the effects on solute excretion. Nephrocalcinosis, which was readily produced in the control animals, was prevented in the experimental animals by pre-treatment with fish oil and urine calcium excretion was significantly reduced. The urinary calcium and oxalate excretion in the recurrent, hypercalciuric stone-formers was significantly reduced with fish oil treatment over an eight week period. There were no untoward side-effects. These studies indicate that the incorporation of EPA in the diet as a substitute metabolic pathway could be a unique way of correcting the biochemical abnormalities of idiopathic urolithiasis.

Topics: Adult; Aged; Animals; Calcium; Disease Models, Animal; Drug Evaluation; Drug Evaluation, Preclinical; Eicosapentaenoic Acid; Female; Humans; Kidney; Kidney Calculi; Male; Microradiography; Middle Aged; Nephrocalcinosis; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains; Recurrence; Spectrophotometry, Atomic

Administration of high doses of vitamin D3 (2,600 IU/100 ml of drinking water) to adult rats, for one month, significantly altered renal function (P less than 0.01) and enhanced renal accumulation of oxalate (71.44 x 18.82 micrograms/g of tissue in treated rats vs 38.87 +/- 11.96 micrograms/g in untreated rats; P less than 0.001), phosphate (1.388 +/- 188 micrograms/g in treated rats vs 870 +/- 171 micrograms/g in untreated rats; P less than 0.01) and calcium (477 +/- 107 micrograms/g in treated rats vs 326 +/- 104 micrograms/g in untreated rats; P less than 0.01). Urinary analyses of principal promotors and inhibitors of lithogenesis revealed high calcium excretion (1,576 +/- 0.419 mg/24 hr in treated rats vs 0.969 +/- 0.214 mg/24 hr in untreated rats; p less than 0.01) and decreased magnesium excretion (0.330 +/- 0.135 mg/24 hr in treated rats vs 0.910 +/- 0.168 mg/24 hr in untreated rats; p less than 0.001). Microscopic calcium deposits were found in the medulla, especially in renal papilla. These results suggested that vitamin D3, when administered at high doses for a long time, may induce nephrocalcinosis and alter renal function.

Topics: Animals; Calcium; Cholecalciferol; Creatinine; Kidney; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Oxalic Acid; Phosphates; Rats; Rats, Inbred Strains; Uric Acid

This study was carried out in order to investigate renal oxalate excretion in a group of normal subjects (n = 40), a group of patients with uremia (n = 52) and a group with nephrolithiasis (n = 34). We found that the mean concentrations of oxalate in the 24-hour urine specimens of both patient groups were below the normal range. Although the renal creatinine clearance (CCR) was significantly decreased in some stone patients (n = 14), decreased renal oxalate clearance was noted only in those patients with severe renal failure. Thus, plasma oxalate was found to be elevated only in patients with chronic renal failure (mean +/- SD, 49.7 +/- 12.4 mumol/l), while the normal value was 17.0 +/- 6.7 mumol/l. The mean tubular excretion fraction of oxalate was also found to increase markedly in uremia with a mean of 26.3 +/- 17.3% (in normal subjects, 11.7 +/- 7.5%), but their mean daily urinary excretion of oxalate decreased to 63.2 mumol/day (mean value of 232.6 mumol/day in normal subjects). A positive correlation was observed between oxalate and creatinine, and between oxalate and calcium excretion, which was not found in normal subjects or patients with kidney stones. In nephrolithiasic patients, the daily excretion of oxalate, calcium and phosphate had no discernible increment and the mean excretory ratio of oxalate, calcium or phosphate to creatinine was all within normal limits. But when the CCR of stone patients was below 80 ml/min, their daily excretion of oxalate and calcium decreased significantly (p less than 0.01) and the excretory ratio of phosphate to creatinine markedly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Calcium; Humans; Kidney; Kidney Calculi; Kidney Failure, Chronic; Male; Metabolic Clearance Rate; Middle Aged; Oxalates; Oxalic Acid

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.

Topics: Adult; Calcium; Calcium Oxalate; Female; Humans; Hyperoxaluria; Jejunoileal Bypass; Kidney Calculi; Kidney Tubules; Male; Middle Aged; Oxalates; Oxalic Acid

1. This study was performed to test the hypothesis that glycosaminoglycans may play an important role in the observed abnormalities in oxalate flux seen in patients with calcium oxalate nephrolithiasis. 2. Oxalate flux rate, erythrocyte membrane glycosaminoglycan content, membrane protein phosphorylation and effect of heparan sulphate on erythrocyte oxalate flux in vitro were studied in control subjects and patients with calcium oxalate nephrolithiasis. 3. In comparison with control subjects, renal stone-formers showed a significantly higher oxalate self-exchange, a lower erythrocyte membrane glycosaminoglycan content and a higher membrane phosphorylation rate. In stone-formers, erythrocyte glycosaminoglycan content correlated inversely with both oxalate flux rate and protein phosphorylation. In vitro, heparan sulphate promoted a significant fall in the rate of oxalate self-exchange. 4. These findings support the hypothesis that a lower erythrocyte membrane content of glycosaminoglycans enhances membrane protein phosphorylation, leading to an increased rate of transmembrane oxalate flux.

Topics: Adult; Blood Proteins; Calcium Oxalate; Erythrocyte Membrane; Erythrocytes; Female; Glycosaminoglycans; Humans; Kidney Calculi; Male; Membrane Proteins; Middle Aged; Oxalates; Oxalic Acid; Phosphorylation

Topics: Adolescent; Adult; Calcium; Circadian Rhythm; Copper; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Phosphorus; Uric Acid

Lipid peroxidation in kidney of rats fed with vitamin B-6 deficient diet for a period of 12 weeks was studied with pair-fed controls. The basal lipid peroxide level as well as the degree of susceptibility to lipid peroxidation in presence of promotors such as NADPH, ascorbate, t-butyl hydroperoxide, Fe2+, Cu2+ and oxalate, were increased in vitamin B-6 deficient kidney. The observed increased lipid peroxidation in vitamin B-6 deficient kidney was correlated with high levels of lipids, copper, iron, calcium and oxalate, low levels of antioxidants and antioxidant enzymes and increased levels of hydroperoxides and hydroxyl radicals.

Topics: Animals; Antioxidants; Calcium; In Vitro Techniques; Kidney; Kidney Calculi; Lipid Metabolism; Lipid Peroxidation; Male; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains; Vitamin B 6 Deficiency

The effect of the calcium antagonist verapamil, and of thiazide, a well accepted treatment in the prevention of calcium oxalate renal stones, were examined in an experimental renal stone model. Calcium oxalate stones were induced by the synthetic metabolite of vitamin D3, the alpha-OH-vitamin D3 plus ethylene glycol fed rats. A significant decrease in urinary calcium and oxalate was observed following verapamil treatment. Thiazide significantly decreased urinary calcium, but unlike verapamil, did not decrease urinary oxalate. However, no differences in the radiological findings or in the calcium or magnesium content of the kidneys were observed. Although several animal models have been described for the study of calcium oxalate stones, none has yet been proven useful for the evaluation of stone therapy.

Topics: Animals; Calcium; Chlorothiazide; Ethylene Glycol; Ethylene Glycols; Hydroxycholecalciferols; Kidney Calculi; Male; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains; Verapamil

Nephrolithiasis occurs in 5 to 13% of patients with ulcerative colitis (UC) who undergo colectomy and abdominal ileostomy, presumably from chronic dehydration and urinary concentration. Whether endorectal ileal pullthrough with ileal reservoir (PTR) changes the incidence of stones (primarily calcium oxalate) after colectomy is not known. Urinary excretion of Na2+, K+, Ca2+, Mg2+, phosphate, urate, oxalate, and citrate was measured in a prospective study of 12 UC patients undergoing PTR with temporary end ileostomy. Twenty-four-hour urine samples were obtained before colectomy (t1), after colectomy but before ileostomy closure (t2), and 5 months after ileostomy closure (t3). Urine volumes decreased from 831 +/- 101 cc (mean +/- SE) at t1 to 715 +/- 101 cc at t2 and then increased to 1278 +/- 421 cc at t3 (significant, with P less than 0.01 by t test). Urinary excretions of Mg2+, oxalate, and citrate were low in UC patients compared to those in controls (15 healthy adult volunteers). Excretion of Ca2+ increased significantly following temporary ileostomy while excretion of Mg2+ fell. Excretion of Ca2+ fell and excretion of Mg2+ and citrate increased following PTR. We conclude that PTR patients have increased urine volumes and urinary ion changes known to decrease the risk of developing renal stones.

Topics: Adolescent; Adult; Citrates; Citric Acid; Colectomy; Colitis, Ulcerative; Electrolytes; Female; Humans; Hydrogen-Ion Concentration; Ileum; Kidney Calculi; Male; Middle Aged; Oxalates; Prospective Studies; Uric Acid

By oral administration of 14C-labelled oxalic acid (2.2 microns Ci; 2 mg), the mean enteral oxalate absorption in 24-h urines (collecting intervals 3, 3, 6, 12 h) of 19 healthy control subjects was determined to be 8.3%. It was 14.6% (alpha less than 1%) in 20 patients with recurrent idiopathic calcium-oxalate lithiasis. The differences in absorption were most marked in the first two 3-h urines. Under the test conditions described, maximum excretion of 14C oxalate had already occurred after 3 h (55%-57%); after 6 h it was about 85%, and after 12 h 95% of the total activity in the 24-h urine. In 68% of the control subjects, the oxalate absorption values were below 10%; in 32% they were less than or equal to 15%. For the group of lithiasis patients, these findings suggest a metabolic disorder of gastrointestinal origin. In 40%, the oxalate absorption rates were clearly above 15%. The test method described is simple to carry out and can be recommended for the assessment of idiopathic calcium-oxalate lithiasis.

Topics: Adult; Calcium Oxalate; Carbon Radioisotopes; Female; Humans; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Oxalic Acid; Recurrence

The difficulties of biochemical diagnosis in children and in chronic renal failure are discussed in detail, as well as the development of diagnostic and therapeutic possibilities in recent years, exemplified by 4 cases. Excretion of oxalate (and glycolate) may be incorrectly assumed to be normal with: a) uncritical application of the method of measurement, b) disregard of the clearly lower oxalate excretion in children (values should be referred to m2 of body surface), c) disregard of a decreased glomerular filtration rate (values should be referred to the creatinine clearance). With compromised renal function the excretion of oxalate and glycolate in primary oxalosis drops to "normal" whereas plasma values increase considerably. In this case the biochemical diagnosis is possible only by measurement of plasma values of glycolate and oxalate. Consequently, extensive extrarenal deposition of calcium oxalate crystals will, as a rule, become clinically manifest only after chronic renal failure has turned irreversible. In recent years, several therapeutic procedures, have been developed. They are of therapeutic significance for the early stages of the disease as well. Observing especially conditions renal transplantation or combined hepatorenal transplantation can be managed with a successful outcome. As the perioxisomal enzyme is activated only in the liver cells, an early liver transplantation as a definitive treatment by enzyme replacement may be the successful therapy in the future.

Topics: Adolescent; Child; Child, Preschool; Female; Follow-Up Studies; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Calculi; Kidney Failure, Chronic; Kidney Function Tests; Kidney Transplantation; Male; Oxalates; Oxalic Acid; Renal Dialysis; Urogenital System

Topics: Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney; Kidney Calculi; Kidney Failure, Chronic; Middle Aged; Oxalates; Skin; Skin Diseases; Vascular Diseases

Circadian rhythmicity in urinary volume and excretion of creatinine, calcium, oxalate, uric acid and phosphate was studied in 15 idiopathic stone formers and in 17 control subjects who were age-matched, related adult males, living in the same house and engaged in similar occupations to those of the stone patients, but who had no clinically obvious stone disease. Three-hourly urine samples were collected and creatinine, calcium, oxalate, uric acid and inorganic phosphate were estimated. The time series of data were analysed by cosinor rhythmometry. Circadian rhythmicity has been described in urinary volume and urinary excretion of creatinine, calcium, oxalate, uric acid and inorganic phosphate in normal subjects, but it was not detected in the stone formers. The control subjects exhibited a circadian rhythmicity only in urinary volume and creatinine excretion. Thus they occupied a position midway between healthy adults, who exhibit circadian rhythmicity in all of the above parameters, and the stone formers, who appear to have lost it altogether.

Topics: Adult; Calcium; Circadian Rhythm; Creatinine; Humans; Kidney Calculi; Oxalates; Phosphates; Uric Acid

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.

Topics: Absorption; Adult; Ascorbic Acid; Calcium; Calcium Oxalate; Calcium, Dietary; Citrates; Citric Acid; Female; Humans; Kidney Calculi; Kinetics; Male; Middle Aged; Oxalates; Oxalic Acid

The effects of oxalate on kidney mitochondria were evaluated in vitro to test whether oxalate exposure leads to derangement(s) in mitochondrial function that could in turn promote the formation of kidney stones. Our previous studies demonstrated that oxalate is transported across the mitochondrial membrane via the dicarboxylate carrier. The present studies indicated that oxalate competitively inhibits the uptake and oxidation of exogenous malate and succinate in isolated mitochondria but has no effect on mitochondrial respiration in the presence of a mixture of glutamate plus malate or glutamate plus pyruvate. Oxalate attenuates the increase in mitochondrial respiration produced by the uncoupler CCCP or by the Ca2+ ionophore A23187, and the latter effect is more pronounced in kidney than in liver mitochondria. The apparent Ki of oxalate for the response to Ca2+ ionophore is 1.9 +/- 0.3 mM in kidney and 6.1 +/- 0.2 mM in liver mitochondria. Similarly, the ability of oxalate to attenuate calcium-induced swelling of mitochondria is more dramatic in kidney than in liver mitochondria (apparent KiS of 1.7 +/- 0.1 and 18.2 +/- 0.7 mM, respectively). Oxalate has no effect on the rate of calcium uptake by energized mitochondria or on the rate of ruthenium red-insensitive calcium efflux from mitochondria in either tissue. The above findings indicate that oxalate interacts with the inner mitochondrial membrane or with processes controlling membrane integrity to a greater extent in kidney than liver mitochondria. The effects of oxalate on membrane permeability or integrity may be more important than its effects on mitochondrial energy production or calcium sequestration in the pathogenesis of calcium oxalate microlith formation in the kidney.

Topics: Animals; In Vitro Techniques; Intracellular Membranes; Kidney; Kidney Calculi; Mitochondria; Mitochondria, Liver; Oxalates; Oxalic Acid; Oxygen Consumption; Rats; Rats, Inbred Strains

The initial part of this presentation deals with the sensitivity of tests commonly used in the diagnosis of primary hyperparathyroidism. Total serum calcium levels often are normal in patients with small parathyroid adenomas but levels of serum ultrafilterable and/or ionized calcium usually are elevated in these patients. The recent introduction of improved radioimmunoassays for measurement of circulating parathyroid hormone has led to greatly improved sensitivity of this test for the diagnosis of primary hyperparathyroidism. However, measurement of total urinary cyclic adenosine monophosphate, even when expressed as a function of glomerular filtration rate, is an extremely insensitive test in patients who have parathyroid adenomas weighing less than 1 gm. Consequently, this test no longer is used for diagnostic purposes in our laboratory. Data relating to the prevalence and causes of hyperoxaluria in patients with idiopathic calcium oxalate stones also are presented. Hyperoxaluria (more than 450 mumol. per 24 hours) was found in 21 of 99 consecutive untreated male patients. Approximately a third of the patients with high normal or increased urinary oxalate excretion also have increased urinary glycolate excretion, which is indicative of increased endogenous oxalate production. This metabolic abnormality was unresponsive to pyridoxine administration but preliminary findings suggest that it may be corrected by restricting dietary protein.

Topics: Calcium; Glycolates; Humans; Hyperparathyroidism; Kidney Calculi; Oxalates; Parathyroid Hormone

A medical history and laboratory investigation of patients with recurrent stones serve as the cornerstone for preventive and therapeutic treatment. Identifiable risk factors can be discovered in 90 per cent of the patients. More sophisticated analyses of urinary supersaturation can be helpful in resistant cases.

Topics: Calcium; Cystine; Humans; Kidney Calculi; Oxalates; Recurrence; Uric Acid; Urinary Tract Infections

The fractional intestinal absorption of oxalate and calcium was investigated by isotope techniques in 20 normal subjects and in 12 idiopathic calcium oxalate stone formers. The greatest amount of 14C-oxalate was excreted during the first six hour period in controls as well as in stone formers. The stone formers had a greater intestinal uptake of oxalate (11 +/- 5.1%) than the controls (6.2 +/- 3.7%; p less than 0.01). There was no significant relationship between the fractional absorption of oxalate and the total urinary oxalate excretion. The stone formers also had a higher fractional uptake of calcium compared to the controls (55 +/- 11% vs. 47 +/- 9.1%; p less than 0.05). There was a positive relationship (r = 0.47) between the urinary excretions of calcium and oxalate in the stone formers. During these conditions no correlation could be demonstrated between the fractional absorptions of oxalate and calcium, neither in the stone formers nor in the controls. In conclusion, patients with recurrent formation of calcium oxalate containing stones appear to have an enhanced intestinal uptake of both oxalate and calcium. This disturbance could be of primary pathogenic importance for their stone forming propensity.

Topics: Adult; Aged; Calcium; Carbon Radioisotopes; Female; Humans; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence

Several methods for the measurement of crystallization conditions in urine, the so-called whole urine systems, have recently been of considerable interest in urolithiasis research. The diagnostic accuracy of the oxalate tolerance value (OTV) was therefore compared with the daily excretion of oxalate and citrate in normal persons and patients with urinary calculi. With the aid of the oxalate/citrate ratio, 77% of the patients could be classified correctly. After standardization of the experimental conditions (24-h urine sample, constant pH value, consideration of endogenous oxalate) we succeeded in correctly classifying 82% of patients using the OTV. These results favour the introduction of the OTV as a clinical chemical tool for the follow-up of patients with urinary calculi and for the screening of normal persons at risk.

Topics: Adult; Calcium Oxalate; Citrates; Citric Acid; Creatinine; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Oxalates; Oxalic Acid; Risk Factors

We wished to determine whether different types of dietary protein might have different effects on calcium metabolism and on the propensity for renal stone formation. Fifteen young normal subjects were studied during three 12-day dietary periods during which their diet contained vegetable protein, vegetable and egg protein, or animal protein. While these three diets were constant with respect to Na, K, Ca, P, Mg, and quantity of protein, they had progressively higher sulfur contents. As the fixed acid content of the diets increased, urinary calcium excretion increased from 103 +/- 15 ( +/- SEM) mg/day (2.6 +/- 0.4 mmol/day) on the vegetarian diet to 150 +/- 13 mg/day (3.7 +/- 0.3 mmol/day) on the animal protein diet (P less than 0.02). Despite the increased urinary calcium excretion, there was a modest reduction of urinary cAMP excretion and serum PTH and 1,25-dihydroxyvitamin D levels consistent with acid-induced bone dissolution. There was no change in fractional intestinal 47Ca absorption. The inability to compensate for the animal protein-induced calciuric response may be a risk factor for the development of osteoporosis. The animal protein-rich diet was associated with the highest excretion of undissociated uric acid due to the reduction in urinary pH. Moreover, citrate excretion was reduced because of the acid load. However, oxalate excretion was lower than during the vegetarian diet [26 +/- 1 mg/day (290 +/- 10 mumol/day) vs. 39 +/- 2 mg/day (430 +/- 20 mumol/day); P less than 0.02]. Urinary crystallization studies revealed that the animal protein diet, when its electrolyte composition and quantity of protein were kept the same as for the vegetarian diet, conferred an increased risk for uric acid stones, but, because of opposing factors, not for calcium oxalate or calcium phosphate stones.

Topics: Adult; Animals; Calcitriol; Calcium; Crystallization; Cyclic AMP; Dietary Proteins; Eggs; Female; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Kidney Calculi; Male; Oxalates; Oxalic Acid; Parathyroid Hormone; Risk Factors; Sulfur; Uric Acid; Urine; Vegetables

Pyridoxine in doses of 250-500 mg daily by mouth was administered to 12 patients suffering from recurrent calcium oxalate renal calculi and idiopathic hyperoxaluria. This therapy decreased urinary oxalate excretion significantly (p less than 0.025) during up to 18 months of treatment. In that period eight patients showed no evidence of active stone disease; three showed slight increase in the size of their old stone(s) and one patient formed one new stone. None of these patients developed any significant complications of the therapy. These findings support the view that pyridoxine in pharmacological doses is useful in the control of elevated urinary oxalate excretion in patients with recurrent renal oxalate calculi.

Topics: Adult; Aged; Female; Humans; Hyperoxaluria; Kidney Calculi; Male; Middle Aged; Oxalates; Pyridoxine

Topics: Calcium Oxalate; Humans; Hyperoxaluria; Kidney Calculi; Male; Oxalates

Topics: Calcium; Calcium, Dietary; Diet; Dietary Proteins; Drinking; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence; Sodium, Dietary

Topics: Apatites; Calcium Phosphates; Combined Modality Therapy; Humans; Kidney; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Phosphates; Struvite

An increased frequency of kidney stone formation is reported in patients with inflammatory bowel disease. In order to investigate its pathogenesis, the concentrations of factors known to enhance calcium oxalate stone formation (oxalate, calcium, uric acid) as well as of inhibitory factors for nephrolithiasis (magnesium, citrate) were determined in the urine of 86 patients with Crohn's disease and compared with those of 53 metabolically healthy controls. Six patients with Crohn's disease already had experienced calcium oxalate nephrolithiasis. Patients with Crohn's disease had significantly higher urinary oxalate and lower magnesium and citrate concentrations. Among all patients magnesium and citrate were significantly lower in those with a positive history of kidney stones. Our results demonstrate that the increased propensity for renal stone formation in patients with Crohn's disease is a result not only of increased urinary oxalate, but also of decreased urinary magnesium and citrate concentrations.

Topics: Adult; Calcium; Citrates; Citric Acid; Crohn Disease; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Phosphates; Risk Factors; Uric Acid

The ultrastructural change in rat kidneys was analyzed after intraperitoneal injection of oxalic acid. This study demonstrates fundamental alterations in the epithelial cells of the proximal convoluted tubules (PCT). At 8 h (group IV), cytoplasmic prolongations (CP) begin to be observed, which fill the lumens of PCT at 20 h (group VII) and 24 h (group VIII). Unusual mechanism of cytoplasmic secretion is suggested to this fact. Calcium salts were found on CP and in group VIII. At 16 h (group IV), intracitoplasmic membranous structures (MS) appear, which can emigrate across the microvilli into the lumens of PCT. At 24 h (group VIII), MS are also shown in basal zone and in basement membrane. We considered that CP, which can fragment, and MS are the ultrastructural substratum of the matrix of the calculis, corresponding probably to the substance A.

Topics: Animals; Kidney; Kidney Calculi; Kidney Tubules; Male; Microscopy, Electron; Oxalates; Oxalic Acid; Rats; Time Factors

Topics: Adult; Calcium; Calcium Oxalate; Creatinine; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

The systematic collection and filtration of urine for three days after extracorporeal shock wave lithotripsy (ECSWL) has enabled the chemical analysis of the stones treated in 90% of cases. We have been able to demonstrate a correlation between the chemical nature and the mode of fragmentation of the stones. Calcium oxalate monohydrate, brushite and cystine stones form fairly large, well separated, angular fragments with sharp edges. Calcium oxalate dihydrate, calcium phosphate and magnesium ammonium-phosphate (struvite) stones are reduced to an amorphous dust. These findings have direct therapeutic implications, as it is absolutely essential to make sure that no large stone fragments are left in the urinary tract after lithotripsy. These elements led us to try to evaluate the chemical nature and the hardness of the stones on the basis of the radiological findings, in order to adopt the best possible therapeutic strategy. Calcium oxalate dihydrate stones have a striated, spiky and non-homogeneous appearance on plain X-rays. They are frequently responsible for filling defects on intravenous pyelography. They are friable stones which are easily fragmented. In contrast, calcium oxalate monohydrate stones present a regular homogeneous opacity on plain X-rays with no filling defect on intravenous pyelography. These stones are hard and are broken up, with difficulty, into large fragments on the initial fluoroscopic images at the start of treatment. Many stones have a mixed composition (calcium oxalate monohydrate, calcium oxalate dihydrate and calcium phosphates): the plain X-ray does not provide sufficient information and the presence of a filling defect on intravenous pyelography may or may not be suggestive of a friable stone.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Calcium Oxalate; Calcium Phosphates; Cystine; Humans; Kidney Calculi; Lithotripsy; Oxalates; Radiography; Uric Acid; Urine

The influence of a calcium-rich mineral water on urine crystallisation in patients with recurring kidney stones was investigated. A calcium and magnesium rich water like the one tested increases the calcium and magnesium content of the urine but decreases oxaluria even after a dietary oxalate load.

Topics: Calcium; Citrates; Crystallization; Diet; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Male; Mineral Waters; Oxalates; Phosphates; Recurrence

Topics: Chromatography, Liquid; Electrochemistry; Electrodes; Humans; Keto Acids; Kidney Calculi; Oxalates

Clinical, radiographic and scintigraphic abnormalities in primary oxalosis of a 52 years old female are demonstrated. Severe oxalosis-nephropathy and oxalosis-arthropathy/enthesiopathy are shown. For the first time an intense myocardial uptake of 99 m Tc-HDP and 99 m Tc-MDP is described in connection with oxalosis. It is suggested that in the appropriate clinical setting this pattern may be suggestive of oxalosis-cardiomyopathy. Review of literature.

Topics: Arthritis; Bone Diseases; Cardiomyopathies; Diphosphonates; Female; Humans; Hyperoxaluria; Kidney Calculi; Middle Aged; Oxalates; Technetium; Technetium Tc 99m Medronate

Selective pharmacologic therapy of calcium nephrolithiasis is highly effective in preventing new stone formation. A remission rate of greater than 80 per cent and overall reduction in individual stone formation rate of greater than 90 per cent can be obtained in patients with calcium nephrolithiasis. In patients with mild-to-moderate severity of stone disease, virtually total control of stone disease can be achieved as evidenced by remission rates of greater than 95 per cent. The need for stone removal may be dramatically reduced by an effective prophylactic program. Selective pharmacologic therapy of calcium nephrolithiasis also encompasses the advantages of overcoming the nonrenal manifestations of conditions that cause stone formation as well as averting certain side effects that may be caused by nonselective medical therapy. Despite these advantages, selective medical therapy clearly cannot provide total control of stone disease. A satisfactory response requires continued, dedicated compliance by patients to the recommended program and a commitment of the physician to provide long-term follow-up and care.

Topics: Benzothiadiazines; Calcium; Cellulose; Citrates; Citric Acid; Diuretics; Humans; Ion Exchange Resins; Kidney Calculi; Oxalates; Phosphates; Sodium Chloride Symporter Inhibitors; Uric Acid

We used a xylitol load to test the two-carbon pathway to oxalate production in humans. Use of this pentose sugar caused a fourfold increase in glycolate excretion, indicating its suitability as a dynamic function test of two-carbon metabolism. However, despite this increase in glycolate excretion in 10 recurrent stone formers and six normal subjects, there was no concomitant increase in oxalate excretion in either group. By comparison, a sucrose load produced no increase in excretion of either glycolate or oxalate. In addition, when we studied four recurrent calcium stone formers on successive diets with various fat content, we found no correlation between high fat intake and increased glycolate or oxalate excretion. In summary, there was no evidence of abnormal fluxes through the two-carbon pathway to oxalate in recurrent stone formers, nor of hyperoxaluria as related to increased intake of sucrose or fat.

Topics: Adult; Calcium Oxalate; Dietary Fats; Female; Glycolates; Humans; Kidney Calculi; Kinetics; Male; Middle Aged; Oxalates; Oxalic Acid; Sucrose; Xylitol

The acute effects of a single (5 g) oral load of sodium potassium citrate (SPC), given together with a liquid test meal, were studied in 6 healthy male volunteers with respect to changes in serum citrate, blood acid base status, urine pH, citrate, calcium and minerals, and oxalate, as well as the calculated relative supersaturation of urine with several stone-forming phases, and the associated crystalluria. It was found that, apart from making the urine more alkaline, SPC induces mild compensated metabolic alkalosis, increases serum and urinary citrate, and reduces fractional urinary calcium excretion, but leaves urinary oxalate and the accompanying crystalluria unchanged. Except for the increase in urinary supersaturation with hydroxyapatite, the supersaturation of other important stone-forming constituents is statistically unchanged. In addition, there are indications that SPC reduces postprandial intestinal calcium absorption without affecting serum parathyroid hormone and 1,25-dihydroxyvitamin D. It is concluded that there is a spectrum of acute effects of oral SPC that may warrant long-term trials on this medication in the metaphylaxis of calcium-containing urinary stones.

Topics: Adult; Calcium; Citrates; Citric Acid; Crystallization; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid

In 43 healthy reference persons and 54 patients with relapsing calcium oxalate nephrolithiasis the absorption of oxalic acid was measured by means of 14C-oxalic acid. In patients with oxalate calculi the absorption of oxalic acid is totally increased and also in such ones with Whewellite-calculi. It is decreased in carriers of Weddelite calculi. The increase of the absorption of oxalic acid in patients with mixed calculi is not significant.

Topics: Adult; Calcium; Calcium Oxalate; Female; Humans; Kidney Calculi; Kidney Tubules; Magnesium; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence

Twenty-two recurrent calcium stone formers had 24-h urinary oxalate excretions on their home diets which were significantly greater than those of 30 normal subjects (0.48 +/- 0.23 mmol/d; mean +/- SD compared with 0.31 +/- 0.11; P less than 0.01). The stone formers also demonstrated marked day to day variability in oxalate excretion indicating that a single normal urinary oxalate measurement did not exclude significant hyperoxaluria at other times. On a hospital diet containing 1000 mg calcium per day, urinary oxalate excretion fell significantly from 0.48 +/- 0.23 mmol/d to 0.32 +/- 0.12; P less than 0.01. As the urinary calcium excretion in and out of hospital was similar, it seems unlikely that low calcium intake at home was responsible for the hyperoxaluria. All patients had recurrent symptomatic stone disease and had been advised to avoid foods rich in oxalate. Whilst poor compliance is a possible explanation for the variability in oxalate excretion, we believe it is more likely that there is an inadvertent intake of oxalogenic precursors in their diet. As normal subjects do not demonstrate hyperoxaluria on similar home diets, stone formers may have a metabolic defect in the handling of these precursors.

Topics: Adult; Aged; Calcium; Calcium, Dietary; Diet; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence

The participation of oxalate in nephrolithiasis was evaluated in 202 stone patients. The activity product and formation product ratios of calcium oxalate were substantially altered in the stone population. Treatment with thiazide derivatives and/or allopurinol was able to decrease urine oxalate and normalize the activity product and formation product ratios. Stone activity decreased in the stone population after treatment. Our data suggest that oxalate may have a critical role in nephrolithiasis activity.

Topics: Allopurinol; Calcium; Calcium Oxalate; Drug Evaluation; Female; Hydrochlorothiazide; Hydrogen-Ion Concentration; Kidney Calculi; Male; Oxalates; Uric Acid

Topics: Adult; Aging; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence; Sex Factors

Topics: Adult; Calcium Oxalate; Erythrocyte Membrane; Female; Flunarizine; Humans; Kidney Calculi; Male; Oxalates; Recurrence

Topics: Adult; Calcium; Calcium Oxalate; Citrates; Diuretics; Female; Glycosaminoglycans; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Oxalic Acid; Quinazolines; Sulfonamides

An investigation of variables important to calcium stone formation in urine indicated significantly increased daily excretion of calcium and oxalate and decreased excretion of ascorbate and citrate by recurrent calcium stone formers. In addition, urine volume, sodium, mucopolysaccharide, and protein were also significantly increased. We compared the uptake of citrate and ascorbate from the gut into the blood in normal controls and stone formers. These studies indicated significantly depressed absorption of both these hydroxycarboxylic acids in recurrent calcium stone formers. We also found that concurrent administration of citrate inhibited ascorbate absorption and increased urinary oxalate excretion after an ascorbate load in normal subjects and stone formers. These findings suggest a mechanism that explains hyperoxaluria in stone patients on the basis of a malabsorption of citrate, ascorbate, and possibly other hydroxycarboxylic acids.

Topics: Absorption; Adult; Ascorbic Acid; Calcium; Citrates; Citric Acid; Female; Humans; Kidney Calculi; Malabsorption Syndromes; Male; Middle Aged; Oxalates; Oxalic Acid; Sodium; Urine

Sodium pyruvate, potassium pyruvate, pyruvic acid, sodium bicarbonate and potassium bicarbonate were added to a calcium-oxalate lithogenic diet (a glycolic-acid diet) in order to determine their effects in preventing lithogenicity. Male Wistar-strain rats who had been fed the glycolic-acid diet developed marked urinary calculi within four weeks. Rats in the sodium and potassium pyruvate groups had, however, almost no stones in the urinary system. Rats in the bicarbonate and pyruvic-acid groups showed slightly less effect than those in the pyruvate groups. Urinary oxalate excretion was high in all the groups during the experiment. The urinary oxalate concentration was relatively higher in the sodium-pyruvate group, and significantly higher in the potassium-pyruvate group, than in the glycolic-acid group. Urinary citrate excretion was high both in the pyruvate and bicarbonate groups; the urinary citrate concentration was, however, significantly higher in the pyruvate groups than in the bicarbonate groups at the fourth experimental week. The urinary calcium and magnesium concentrations were irrelevant to the diets administered. Therefore, it can be concluded that pyruvate salts inhibit urinary calculi formation, not by decreasing oxalate synthesis, but by increasing the urinary citrate concentration; bicarbonate salts work in the same manner, but a little less effectively.

Topics: Animals; Bicarbonates; Calcium; Citrates; Diet; Glycolates; Hydrogen-Ion Concentration; Kidney; Kidney Calculi; Magnesium; Male; Oxalates; Potassium Compounds; Pyruvates; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Urinary Calculi

Primary hyperoxaluria is a rare metabolic disorder characterized by excessive synthesis and urinary excretion of oxalate. Nephrocalcinosis with or without calcium oxalate nephrolithiasis leads to renal failure in infancy through young adulthood. Oxalosis is the condition in which the highly insoluble calcium oxalate crystals are deposited in extrarenal tissues including bone, blood vessels, heart, and the male urogenital system. The radiographic abnormalities in 14 patients with primary hyperoxaluria are described. These abnormalities include nephrolithiasis, nephrocalcinosis, dense vascular calcifications, abnormal bone density, and characteristic metaphyseal abnormalities. Changes of renal osteodystrophy and pathologic fractures are common. Radiographic bone abnormalities are dependent on the age of the patient when renal failure occurred and the degree of success of renal transplantation. Characteristic skeletal changes are present in six of seven patients who developed renal failure when less than 7 years of age.

Topics: Adolescent; Adult; Calcinosis; Child; Child, Preschool; Female; Fractures, Spontaneous; Humans; Infant; Kidney Calculi; Male; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates; Radiography; Vascular Diseases

Topics: Adult; Alkaline Phosphatase; Circadian Rhythm; Electrolytes; Female; Humans; Hydroxyproline; Kidney Calculi; Male; Oxalates; Oxalic Acid; Uric Acid

Topics: Calcium; Calcium Oxalate; Citrates; Female; Humans; Kidney Calculi; Male; Oxalates; Sex Factors; Software; Uric Acid

Topics: Adult; Calcium; Calcium Oxalate; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Oxalates

Chemical findings were obtained from 24 h urine samples of 43 male calcium-oxalate stone-formers on an unrestricted diet. Results were compared with data from 51 age-matched healthy blood donors. No differences were found in the excreted quantities of calcium, oxalic acid, uric acid and inorganic phosphate, nor in the calcium to creatinine ratio or the activity product of calcium and oxalic acid. The only differences were a higher output of magnesium and a higher magnesium to calcium ratio for controls. The extent of these differences, however, does not justify further subdivision of the group of stone-formers. The diagnostic and therapeutic significance of the chemical analysis of one 24 h urine sample is doubtful for this group of patients.

Topics: Adult; Calcium; Calcium Oxalate; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Middle Aged; Oxalates; Phosphates; Recurrence; Time Factors; Uric Acid; Urine

Topics: Calcium; Humans; Kidney Calculi; Nifedipine; Oxalates; Oxalic Acid

The dietary intakes of 88 renal stone cases and 88 age and sex matched controls were assessed by dietary history using a standardised questionnaire. The stone cases were divided into six subgroups established on the basis of urine biochemistry (calcium, oxalate and uric acid) and stone composition. The average intake of each group was then compared with that of their controls using standard statistical procedures. Cases with idiopathic calcium oxalate stones had significantly lower intakes of dietary fibre, non-cellulose polysaccharide, phytate, magnesium, phosphate and thiamine than controls. No significant difference in dietary intake was found between cases with high urinary calcium and uric acid and their respective controls. All cases with a high urinary oxalate had a significantly higher intake of vitamin C than controls. Our results support the belief that dietary intake is an important pre-urinary risk factor of idiopathic renal stone disease.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Diet; Female; Humans; Kidney Calculi; Male; Oxalates; Risk; Sex Factors; Uric Acid

Topics: Animals; Calcium; Fishes; Food Handling; Humans; India; Kidney Calculi; Magnesium; Oxalates; Oxalic Acid; Phosphorus; Rats; Vegetables

This study is presented as a debate on nephrolithiasis by a urologist and an internist. The reason is that in 1986 the urologist has become successful at desintegrating almost any stone without open surgery, whereas the internist's approach to the same problem is entirely based upon an understanding of pathophysiological mechanisms. After having reviewed the major risk factors for renal stone disease, i.e. small urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, very high or very low urine pH and hypocitraturia, the author shows that now it is not only possible to selectively correct each of these disorders, but that in doing so the internist does change the natural history of the disease. For instance, definite remissions have been obtained by advising patients to increase water intake, by administering thiazides to hypercalciurics, pyridoxine to some hyperoxalurics, allopurinol to hyperuricosurics, urease inhibitors to struvite stone formers and citrate to hypocitraturics. Therefore, the author concludes that the role of the urologist and that of the internist are complementary: although the former now desintegrates the stone without open surgery, the latter, who takes care of the same patient next, is now largely able to prevent relapse of nephrolithiasis after determining the cause of the disease.

Topics: Calcium; Citrates; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Risk; Uric Acid

Topics: Adolescent; Calcium Oxalate; Child, Preschool; Female; Humans; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Oxalic Acid; Radiography

Topics: Adult; Drug Therapy, Combination; Female; Humans; Kidney Calculi; Oxalates; Oxalic Acid; Pyridoxine; Succinimides

We have performed a multivariate analysis of urine abnormalities in patients with calcium oxalate nephrolithiasis, in which effects of gender were also considered. The characteristic of patients that most clearly sets them apart from normal people is a high level of urine calcium for any given level of urine citrate. Other urine measurements cannot improve upon the separation between patients and normals provided by urine calcium and citrate, and their abnormal relationship to each other. Normal women have higher urine citrate and lower urine calcium than normal men or patients of either sex; normal men differ from stone forming men only moderately. Direct measurements of supersaturation are not helpful in distinguishing between patients and normals, once calcium and citrate have been considered. From our analysis, we have derived a new index for evaluating the significance of urine calcium and citrate levels that seems to offer a better basis for clinical diagnosis than criteria presently in use.

Topics: Calcium; Citrates; Citric Acid; Female; Humans; Kidney Calculi; Male; Oxalates; Oxalic Acid; Regression Analysis; Sex Factors; Sodium; Uric Acid

There is evidence to suggest that sucrose ingestion can cause renal parenchymal changes as well as increasing the urinary saturation index for calcium oxalate. Ten stone formers and 10 normal subjects received 250 gm of sucrose daily over a period of 7 days. Observations on the risk factors for calcium stone formation and urinary N-acetyl-B-glucosaminidase (NAG), a marker of renal tubular cell damage, were made. Oxalate excretion increased. Urinary calcium levels were unchanged but the pattern of response was different between the two groups, as with magnesium and phosphate. NAG was spontaneously higher in the patient group and increased significantly after sucrose ingestion in both groups.

Topics: Acetylglucosaminidase; Adult; Calcium; Humans; Kidney; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Oxalic Acid; Phosphates; Sucrose; Urination

Topics: Adult; Calcium; Calcium, Dietary; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate. It is not known, however, whether pyridoxine would equally influence hyperoxalurias of other origins, e.g. idiopathic or enteric. Two groups of patients were therefore given pyridoxine orally for 2 months (300 mg/d). Group 1 consisted of 10 idiopathic stone formers with mild hyperoxaluria of unknown origin. Group 2 consisted of 4 patients with enteric hyperoxaluria after intestinal bypass surgery. As a mean, enteric hyperoxaluria was not influenced by vitamin B6, which suggests that this disorder is the consequence of intestinal hyperabsorption of oxalate rather than of glyoxylate. In contrast, idiopathic hyperoxaluria was influenced by vitamin B6: urinary excretion of oxalate decreased in 8 patients out of 10 and became normal in 7. However, two patients did not respond to pyridoxine; both had concomitant severe hyperuricosuria (greater than 1 g/24 h), an observation suggesting that in these cases hyperoxaluria was of dietary origin. Four of the patients whose urinary excretion of oxalate became normal while on pyridoxine were followed up for 8 to 36 months after treatment: in all of them oxaluria remained normal. One whose oxaluria had returned to the upper normal limit was retreated after 2 years and again displayed a fall in urinary oxalate. It is concluded that pyridoxine given to idiopathic hyperoxalurics may correct the disorder, as in primary hyperoxaluria of type I; this is not the case in enteric hyperoxaluria. The mechanisms governing this sensitivity to vitamin B6 remain to be clarified.

Topics: Adult; Drug Evaluation; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Jejunoileal Bypass; Kidney Calculi; Male; Middle Aged; Oxalates; Postoperative Complications; Pyridoxine; Time Factors

Topics: Calcium; Citrates; Diet; Humans; Kidney Calculi; Oxalates; Uric Acid

Studies of recurrent stone formers indicated that they have significantly increased urinary oxalate and decreased ascorbate excretions. Results of oral and intravenous administration of ascorbate indicate an enhanced production of oxalate from ascorbate in recurrent calcium stone formers as compared with normal persons and that most of this oxalate is generated in the gut.

Topics: Adult; Ascorbic Acid; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Time Factors; Urinary Calculi

The inhibitory activity of whole urines from 32 healthy subjects and 50 calcium oxalate renal stone formers was assessed in terms of their ability to withstand increasing quantities of oxalate before undergoing spontaneous nucleation of calcium oxalate, and their response to a standard 30-mumol challenge of oxalate above their measured metastable limits. The concentrations of calcium (p less than 0.05), oxalate (p less than 0.05), urate (p less than 0.01) and glycosaminoglycans (p less than 0.005) were significantly lower in the stone formers than in the controls and were associated with a significantly higher 24-h urinary volume (p less than 0.001). The majority of urine samples precipitated envelope crystals of calcium oxalate dihydrate, while the remainder precipitated the monohydrate. A significantly (p less than 0.02) greater proportion of the urines from stone formers than from controls deposited calcium oxalate monohydrate, and this was attributed to a lower concentration of calcium in these urines. The minimum amounts of oxalate necessary to induce crystal nucleation did not differ between the two groups, but when the measured metastable limits were expressed as the product of the total (i.e. endogenous + that added to induce nucleation) concentrations of oxalate and calcium at which precipitation occurred, then these limits were significantly lower (p less than 0.05) in the stone formers than in the healthy subjects. However, when the metastable limits of a subgroup of stone formers and controls matched for 24-h urinary volume and calcium and urate concentrations were compared, no differences between the groups could be discerned.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Calcium; Calcium Oxalate; Chemical Precipitation; Crystallization; Female; Glycosaminoglycans; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Oxalates; Oxalic Acid; Uric Acid; Urine

We measured the rate of oxalate flux across the red-cell membrane in the steady state in 114 patients with a history of calcium oxalate kidney stones and in 25 controls. Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria. Oxalate exchange was significantly higher in the 98 patients with idiopathic stone formation than in the controls (-1.10 +/- 0.95 [SD] X 10(-2) min-1 vs. -0.31 +/- 0.12 X 10(-2); P less than 0.001); it was above the upper limits of normal in 78 of these patients. All 8 patients with hyperparathyroidism and the patient with primary hyperoxaluria had values in the normal range; 2 of the patients with renal or urinary tract malformation had values at the upper normal limit. A study of five families indicated that the abnormality is an autosomal monogenic dominant trait with complete penetrance and variable expressivity. Oxalate-tolerance tests were carried out in five pairs of brothers. One brother in each pair had the abnormality in oxalate flux, and had a significantly higher percentage of oxalate excretion at two hours after oxalate loading (18.09 +/- 3.07 [SD] vs. 10.37 +/- 3.08 percent; t = 3.97; P less than 0.005) and four hours (14.87 +/- 2.91 vs. 9.89 +/- 2.93 percent; t = 2.70; P less than 0.05). Treatment with oral hydrochlorothiazide (50 mg per day) or amiloride (5 mg per day) or both restored normal or nearly normal red-cell oxalate exchange in all of 33 patients who initially had increased rates. We conclude that an inherited cellular defect in oxalate transport may be a factor in "primary" calcium oxalate stone formation and that this defect may be corrected with diuretics.

Topics: Adolescent; Adult; Amiloride; Biological Transport; Calcium Oxalate; Child; Child, Preschool; Diuretics; Drug Tolerance; Erythrocytes; Female; Humans; Hydrochlorothiazide; Kidney Calculi; Male; Middle Aged; Models, Biological; Oxalates; Pedigree

This report describes studies performed over an 11 year period in a 13 year old girl with hyperoxaluria and calcium oxalate nephrolithiasis who did not have primary hyperoxaluria or any of the recognized causes of secondary hyperoxaluria. The patient also had increased urinary excretion of calcium and magnesium and hyperabsorption of dietary calcium and magnesium. It is suggested that the hyperoxaluria resulted from hyperabsorption of dietary oxalate secondary to hyperabsorption of dietary calcium. Hyperabsorption of dietary magnesium and increased urinary magnesium excretion have not previously been reported in this context. Stone formation ceased and urinary oxalate excretion gradually fell to normal during long term thiazide therapy but hyperoxaluria recurred when orthophosphate therapy was substituted for the hydrochlorothiazide. This is the first report of normalization of urine oxalate excretion during thiazide therapy in a patient with frank hyperoxaluria.

Topics: Adolescent; Calcium; Calcium Oxalate; Female; Follow-Up Studies; Humans; Hydrochlorothiazide; Kidney Calculi; Magnesium; Oxalates

Six children with inflammatory bowel disease and nephrolithiasis are reported. Their mean age at the passage of the first stone was 12.5 years and the mean duration of active inflammatory bowel disease was 34.5 months. Four had ulcerative colitis and two had Crohn's disease. In three patients, the onset of stone disease was associated with a flare in the bowel disease. Stone passage in four patients was accompanied by an increase in abdominal pain; three experienced gross hematuria. Stones from four of the patients were composed primarily of calcium phosphate; stones from the remaining patients contained uric acid and/or calcium oxalate. The pathogenesis of nephrolithiasis as it relates to inflammatory bowel disease is considered and an approach to therapy offered.

Topics: Adolescent; Calcium; Calcium Phosphates; Child; Citrates; Citric Acid; Colitis, Ulcerative; Crohn Disease; Crystallization; Diphosphates; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Uric Acid

Topics: Calcium Oxalate; Erythrocyte Membrane; Female; Humans; Kidney Calculi; Kinetics; Male; Oxalates; Reference Values

Combination of 1 alpha(OH) D3(vit D) and ethylene glycol induced renal or ureteral stones or both consisting of calcium oxalate in male Wistar rats. This study investigates the effect of EHDP on calcium oxalate stone using the rat model. EHDP reduced the frequency of renal stone and calcium content in the kidney, and reduced the size of the stones in the renal pelvis and ureter. EHDP biochemically ameliorated renal injury induced by vit D and ethylene glycol. EHDP suppressed urinary excretion of calcium even though serum calcium slightly increased. EHDP had a phosphaturic action. EHDP elevated urinary excretion of magnesium. However, the severity of hypermagnesuria decreased in the rat which was not given EHDP concomitantly. Although EHDP slightly elevated urinary excretion of oxalate in the control rat, it did not affect the high level of urinary oxalate in the vit D/ethylene glycol rat. EHDP did not produce any histological change in the kidney or femoral bone. These data indicate that EHDP can suppress renal stone formation in the vit D/ethylene glycol rat. It is speculated that firstly, EHDP may physicochemically inhibit stone formation in the process of nidus, aggregation and crystal growth of calcium oxalate, under the supersaturated condition of calcium oxalate in the urine, and secondly, EHDP may endocrinologically inhibit production of 1,25 (OH)2 vit D in the kidney or inhibit 1, 25 (OH)2 vit D-mediated intestinal calcium absorption. It is suggested that in order to prevent stone recurrence, EHDP may be clinically applied not only to calcium phosphate stones but also to calcium oxalate stones and hypercalciuria mediated by an active form of vitamin D.

Topics: Animals; Blood Urea Nitrogen; Calcitriol; Calcium; Calcium Oxalate; Ethylene Glycols; Etidronic Acid; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Phosphates; Rats; Rats, Inbred Strains

The pre-operative urine, pelvic urine, removed calculi and calculus washings were examined bacteriologically in 24 patients undergoing removal of intrarenal calculi. Four of seven patients with struvite calculi had an infected pre-operative midstream urine specimen and six of the seven removed calculi demonstrated significant bacterial growth. Proteus mirabilis was the commonest organism isolated. Of 17 patients with oxalate calculi only one had an infected pre-operative urine culture, but in four cases the removed stones were infected. Quantitative bacteriological culture of the stones and their washings demonstrated that infection is within the stone itself. Pre-operative urine culture failed to predict infection within the stone in 60% of patients with infected stones. The results suggest that the presence of infected urine together with the presence of renal calculus is indication for removal of the calculus.

Topics: Adult; Aged; Bacteriuria; Enterobacteriaceae Infections; Enterococcus faecalis; Escherichia coli; Female; Humans; Kidney Calculi; Klebsiella pneumoniae; Magnesium; Magnesium Compounds; Male; Middle Aged; Oxalates; Oxalic Acid; Phosphates; Proteus; Pseudomonas aeruginosa; Pseudomonas Infections; Staphylococcal Infections; Staphylococcus aureus; Streptococcal Infections; Struvite

Urinary oxalate excretion was measured in 101 male idiopathic calcium (Ca) stone formers studied on 3 dietary conditions (free-choice, Ca-enriched, and low-Ca diet). The population consisted of 38 normocalciuric and 63 hypercalciuric patients. Mean oxalate excretion was similar in normocalciuric and in hypercalciuric patients, on free-choice as well as on Ca-enriched diet. In both conditions the incidence of hyperoxaluria (greater than or equal to 435 mumol/24 h) within each group of stone formers was also similar, ranging from 11 to 22%. On low-Ca diet, however, mean oxalate excretion increased significantly (p less than 0.01) in hypercalciurics but not in normocalciurics; on this diet, the incidence of hyperoxaluria was particularly high in the hypercalciurics (33%), compared with the normocalciurics (13%). On low-Ca diet, oxalate excretion was positively correlated with the estimated degree of intestinal absorption of calcium (p = 0.01). These results show that among idiopathic stone formers, mild hyperoxaluria is not a rare finding and that this disorder can be encountered in each group of patients; its incidence, however, is influenced by the calcium content of the diet. On a low-Ca diet, patients with intestinal Ca hyperabsorption are particularly prone to develop hyperoxaluria, an observation which leads to question the relevance of such a dietary advice unless oxalate intake is simultaneously reduced.

Topics: Adult; Aged; Calcium, Dietary; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

We measured urinary oxalate and glycolate excretion before and during pyridoxine administration (2 to 200 mg per day) in four patients with primary hyperoxaluria. In two patients with type I primary hyperoxaluria, urinary oxalate and glycolate excretion fell markedly in response to a physiologic dose of pyridoxine of 2 mg per day and became completely normal when the dose was increased to 25 mg per day. In the other two patients, who had a different type of primary hyperoxaluria (normal urinary glycolate excretion), there was no response to 2 mg of pyridoxine per day. In one of these patients, doses of 25 and 50 mg per day were also ineffective, but a moderate reduction in oxalate excretion took place with 200 mg per day; in the other patient there was a moderate reduction in oxalate excretion with 25 mg of pyridoxine per day. Our findings suggest that the degree of hyperoxaluria in this disorder may be only slight or moderate if the patient has been ingesting a pyridoxine-rich diet or multivitamin tablets containing small amounts of pyridoxine. Our results also suggest that smaller doses of pyridoxine than those heretofore employed should be tried in patients with primary hyperoxaluria.

Topics: Child; Female; Glycolates; Humans; Kidney Calculi; Metabolism, Inborn Errors; Oxalates; Oxalic Acid; Pyridoxine

Kidney stones in patients with inflammatory bowel disease are usually composed of calcium oxalate. Two factors are important in the increased absorption of dietary oxalate which is responsible for those stones: 1) increased absorption of oxalate in the presence of steatorrhea, and 2) increased permeability of the colon to oxalate. Fortunately, some of the physiologic abnormalities can be corrected. A therapeutic approach is detailed.

Topics: Calcium Oxalate; Calcium, Dietary; Colon; Humans; Inflammation; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Oxalates; Oxalic Acid

Topics: Adult; Aged; Calcium; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Magnesium Compounds; Male; Middle Aged; Oxalates; Parathyroid Hormone; Phosphates; Struvite; Uric Acid

Principally the formation of urinary calculi in children is not very different from that of grown-ups. For children some factors, however, are of special relevance namely recurrent urinary tract infections and malformations in the area of the urinary tract. In western countries nowadays the incidence rate of urinary stones in children is 3-5% of all patients suffering from this disease, in the underdeveloped countries we have rates of about 30%. A clear sex preference in children wasn't found, the age distribution shows that for half of the children suffering from calculi, diagnosis has been made until they've reached school age. Stone localisation is shifting towards the upper urinary tract, in the past we had mainly urinary bladder stones. Concrements containing oxalate are being found more often today. For children we have a high proportion of mixed concrements. The rate of recurrence for children is 15-25%. Diagnostically we have to search out especially for malformations respectively obstructions of the urine flow, disturbances in metabolism in consideration of metaphylaxis possibilities, however, must not be taken out of account either. Promotory and inhibitory factors of stone formation are presented and their significance is explained by means of selected cases of our own patients. Modern techniques of operative resp. instrumental removal of urinary calculi are presented, especially the relevance of modern strategies as e.g. the extracorporal shock wave lithotripsy, percutaneous litholapaxy and ureterorenoscopy are discussed. Adequate metaphylaxis (general, dietetic, medicamentous) can lower the rate of recurrence of stone formation. This is only possible, however, on condition of a consequent diagnosis to find possible causes of stone formation to be able to choose the right measures of metaphylaxis.

Topics: Calcium; Child; Chronic Disease; Humans; Kidney; Kidney Calculi; Oxalates; Oxalic Acid; Pressure; Urea; Ureteral Calculi; Uric Acid; Urinary Tract Infections; Urodynamics

Pure calcium oxalate monohydrate lithiasis is rare--about 5 to 10% of total renal lithiases. The proportion is the same in men and women. Pure calcium oxalate stones are a polished dark brown color, and are very hard. They are visualized radiologically as regular and homogeneous. From a biological standpoint, this type of stone is frequently associated with normal calciuria and oxaluria. Pure calcium oxalate monohydrate stones rarely evolve.

Topics: Adult; Calcium; Calcium Oxalate; Diagnosis, Differential; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Radiography

Topics: Calcium Metabolism Disorders; Female; Humans; Kidney Calculi; Male; Oxalates; Oxalic Acid; Phosphates; Uric Acid

Topics: Benzothiadiazines; Cellulose; Diuretics; Female; Humans; Kidney Calculi; Magnesium Hydroxide; Magnesium Oxide; Male; Oxalates; Oxalic Acid; Phosphates; Sodium Chloride Symporter Inhibitors

Topics: Adult; Diet; Electrolytes; Humans; Intestinal Absorption; Kidney Calculi; Male; Oxalates

The 14C-oxalate clearance was determined in 13 healthy subjects and 22 patients with various diseases and varying degrees of renal function impairment, including 5 patients with primary hyperoxaluria (PH). The clearances of oxalate (Cox) and creatinine (Ccr) were correlated (r = 0.95). The regression line intersects the ordinate at the origin, while the regression coefficient is 2.0. This implies that the fractional Cox is constant, irrespective of the underlying disease and the degree of renal failure. Plasma oxalate (Pox), as calculated from the urinary oxalate excretion (Uox) and Cox, was elevated in patients with severely impaired kidney function and those with PH. Plasma creatinine (Pcr) and Pox were correlated as well (r = 0.83). Pox values of patients with PH were above the 95% confidence limits of the regression line. It is of practical importance that Pox can be estimated from Uox and Ccr when a 14C-oxalate clearance test cannot be performed. The reasons for the constancy of the Cox/Ccr ratio are discussed, and it is suggested that the effective renal plasma flow (ERPF) is the regulating factor for the tubular secretion of oxalate.

Topics: Adolescent; Adult; Creatinine; Female; Humans; Kidney Calculi; Kidney Diseases; Male; Middle Aged; Oxalates; Oxalic Acid

As calcium oxalate stones are the most important component in urolithiasis, an experimental model has to be designed to clarify the pathogenesis and aid in their prevention. Hyperoxaluria as well as hypercalciuria were produced in rats by administering ethylene glycol (0.5%, in drinking water administered ad libitum) and 1-alpha (OH) D3 (0.5 micrograms/rat given every other day), respectively, for three to four weeks. Neither drug alone produced stones efficiently as did the combination regimen of these two compounds. The occurrence of stones was 77.3%, and with only a moderate degree of renal functional impairment. Biochemical and histological data were obtained using this model.

Topics: Animals; Calcium; Calcium Oxalate; Ethylene Glycols; Hydroxycholecalciferols; Kidney; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Rats; Rats, Inbred Strains; Ureteral Calculi; Urinary Calculi

From the analysis of various urinary constituents and the estimation of urinary saturation of stone-forming salts, it is now possible to identify risk factors responsible for or contributing to stone formation. Metabolic factors included calcium, oxalate, uric acid, citrate and pH. Environmental factors were total volume, sodium, sulfate, phosphate and magnesium. Physicochemical factors represented saturation of calcium oxalate, brushite, monosodium urate, struvite and uric acid. A scheme for graphic display of risk factors was developed to allow ready visual recognition of important risk factors presumed to cause stone formation. This graphic display had diagnostic use as well as practical value in following response to treatment. For example, a low urinary pH and high urinary concentration of undissociated uric acid could be discerned readily in cases of uric acid lithiasis, as were high urinary pH and exaggerated urinary supersaturation of struvite in cases of infection lithiasis. In a patient with absorptive hypercalciuria and hypocitraturia treatment with thiazide and potassium citrate could be shown to abolish high risks (hypercalciuria, hypocitraturia and relative supersaturation of calcium oxalate) displayed before treatment.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Citrates; Citric Acid; Humans; Hydrochlorothiazide; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Oxalic Acid; Phosphates; Risk; Struvite; Uric Acid

Patients with recurrent kidney stone disease or stone formers at increased risk of recurrence deserve a thorough metabolic workup. This should be based on a careful history and include urinalysis, serum chemistry studies, and analysis of 24-hour urine collections. Measures to prevent recurrent stone formation are aimed at correcting the metabolic imbalances detected in the workup. A variety of drugs are available that target one or more of the metabolic abnormalities that may be involved. For "surgically active" renal and ureteral stone disease, newer techniques make surgery unnecessary in most cases. Extracorporeal shock wave lithotripsy is becoming the preferred technique for disintegration of upper urinary tract stones. Percutaneous ultrasonic lithotripsy and electrohydraulic disintegration also are widely used. For lower urinary tract stones, the ureteroscope permits either extraction under visualization or ultrasonic disintegration.

Topics: Allopurinol; Benzothiadiazines; Calcium; Cellulose; Citrates; Citric Acid; Cystoscopy; Diuretics; Fluid Therapy; Fluoroscopy; Humans; Kidney Calculi; Lithotripsy; Medical History Taking; Minerals; Oxalates; Phosphates; Pyridoxine; Sodium Chloride Symporter Inhibitors; Ureteral Calculi; Uric Acid; Urine

Among the various treatments for renal calcium stone disease, none has been documented to reduce urinary oxalate. Methenamine-hippurate (Hiprex) has been used extensively in the treatment of urinary tract infections and from micropuncture studies in the rat, using para-aminohippurate, it could be expected to reduce the renal secretion of oxalate. A daily dose of 3 g was given orally to 15 healthy subjects for 2 weeks. However, there was no net decrease in the urinary excretion of oxalate, but a risk index based on the urinary content of calcium, magnesium, oxalate, citrate and urine became reduced during treatment. The urinary inhibition of calcium oxalate crystal growth was unaffected. It is concluded that there may be a potential in methenamine-hippurate for the treatment of calcium stone disease, which can only be evaluated, however, by a clinical trial in stone patients.

Topics: Anti-Infective Agents, Urinary; Calcium Oxalate; Crystallization; Female; Hippurates; Humans; Kidney Calculi; Male; Methenamine; Oxalates; Oxalic Acid; Risk

Cocoa is a strong carrier of oxalic acid (average: 400 mg per 100 g). In three calcium oxalate stone formers clinical observation had been suggestive of excessive intake of cocoa products contributing to calculus formation. We studied the effect on renal oxalate excretion of an oral cocoa load (30 g per m2 body surface given on 2 consecutive days) in 12 former stone formers (group 1), 14 children with isolated microscopic haematuria (group 2), 13 healthy boys (group 3), and 12 healthy girls (group 4). A new enzymatic method was used to measure oxalic acid in cocoa products as well as in urine samples by a two step reaction: 1. Oxalate decarboxylase, 2. formiate dehydrogenase with photometry of NADH. In addition, the daily excretion of the following substances was measured: Citrate, magnesium, and calcium. There was a significant increase of urinary oxalate excretion from an average of 14.5 mg/24 hours before to an average of 22.2 mg/24 hours after the load in healthy children, and a similar increase in stone formers, but not in children with microscopic haematuria. The excretion of citrate and magnesium did not change following cocoa intake. The calcium excretion was higher in stone formers than in the other groups, but the difference was significant only compared to group 2. It is concluded that the risk of calculus formation may increase following continuous and excessive intake of cocoa products in children with a tendency toward hypercalciuria. Counselling of the stone formers resulted in a marked drop of the daily oxalate excretion, and there was no recurrence of calculus formation over a period of 6 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Beverages; Cacao; Calcium; Calcium Oxalate; Candy; Child; Child, Preschool; Citrates; Citric Acid; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid; Plants, Edible

Pyridoxilate is a salt formed from glyoxylic acid and pyridoxine. It has been used therapeutically as an antianoxic drug in the treatment of various arterial complaints. Its use is based theoretically on its ability to block the conversion of glyoxylic acid into oxalic acid. The following cases suggest, however, that pyridoxilate can cause stones. Intraperitoneal injection of glyoxylate in doses of 130 mg/kg will cause oxalate stones in rats. The same effect results from injection of 427 mg/kg pyridoxilate (i.e. an equivalent dose of glyoxylate). In human subjects, intravenous injection of 200 mg of pyridoxilate results in a fourfold increase in the urinary oxalic acid content in the two hours following the injection. Thirteen cases of chronic progressive oxalate stone disease have recently been reported in patients receiving a prolonged course of pyridoxilate at 450 to 600 mg daily. Eight of these patients had no previous history of lithiasis. Oxaluria levels of 80 to 100 mg daily are observed in all cases of lithiasis in patients receiving pyridoxilate. The levels fell after cessation of the pyridoxilate treatment, and reverted to normal (30 mg/24 hours) in all but three patients. These three patients maintained levels of close to 50 mg and all three had a previous history of urolithiasis.

Topics: Aged; Animals; Arterial Occlusive Diseases; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Pyridoxine; Rats; Urinary Calculi

The authors report a case of acute renal failure with hyperoxaluria and intratubular deposits of oxalate crystals, following a massive ingestion of piridoxilate. Cases of calciumoxalate urolithiasis have also been reported after chronic administration of piridoxilate.

Topics: Acute Kidney Injury; Adult; Humans; Kidney; Kidney Calculi; Male; Metabolic Diseases; Oxalates; Pyridoxine

We evaluated the efficacy of selective treatment in 126 patients with recurrent calcium urolithiasis who were chosen on the basis of ability to correct underlying physiochemical disturbances. Patients with hyperparathyroidism underwent an operation. Patients with renal hypercalciuria were treated with thiazide and those with absorptive hypercalciuria were given a low calcium, low oxalate diet with or without thiazide. The only treatment for normocalciuric patients was high fluid intake, which was suggested also to the other groups. A significant individual mean reduction in stone formation was observed in all groups after 5 years of treatment. However, only 48 per cent of the normocalciuric patients were in remission after 5 years of high fluid intake therapy and 45 per cent of those with absorptive hypercalciuria were free of recurrence with diet only. Thiazide treatment seemed to be effective despite the type of hypercalciuria. The effect of the treatment on stone formation was mediated through reduction of risk factors in the urine. Conversely, a high level of risk factors commonly predicted stone recurrence.

Topics: Adult; Aged; Benzothiadiazines; Calcium; Calcium, Dietary; Cyclic AMP; Diuretics; Female; Fluid Therapy; Humans; Hyperparathyroidism; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Parathyroid Glands; Recurrence; Sodium Chloride Symporter Inhibitors; Time Factors; Uric Acid

Red-blood-cell transmembrane oxalate flux was measured in a group of patients with idiopathic calcium oxalate nephrolithiasis and in normal controls. The mean transmembrane oxalate flux rate was significantly higher in stone-forming patients than in controls (0.93 +/- SD 0.31/min vs 0.29 +/- 0.11/min). 80% of stone-forming patients showed raised (greater than 2SD above the mean in controls) transmembrane oxalate flux. Anomalous cellular oxalate transport may be an important pathogenetic factor in calcium oxalate nephrolithiasis.

Topics: Adult; Biological Transport; Calcium Oxalate; Erythrocyte Membrane; Erythrocytes; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

Topics: Anion Exchange Protein 1, Erythrocyte; Erythrocyte Membrane; Humans; Kidney Calculi; Oxalates

Topics: Creatinine; Graft Rejection; Humans; Hypertension; Kidney Calculi; Kidney Transplantation; Male; Middle Aged; Oxalates; Prednisone; Pyelonephritis

The bacteriological status of the pre-operative urine, removed calcium and the pelvic urine was studied in 63 consecutive patients undergoing removal of intrarenal calculi. The overall infection rates in the pre-operative urine, removed calculi and pelvic urine were 29%, 38% and 30% respectively. In patients with staghorn calculi, 58% of patients had an infected pre-operative M.S.S.U., and 82.5% of removed calculi demonstrated significant bacterial growth, with Proteus mirabilis being the predominant organism isolated. In patients with single or multiple oxalate calculi, 17% had an infected pre-operative M.S.S.U., and 22% of removed calculi demonstrated a significant bacterial growth. The findings would indicate that the presence of a positive M.S.S.U. in a patient with a renal calculus is an indication for surgical removal.

Topics: Adult; Aged; Bacteriuria; Female; Humans; Kidney Calculi; Magnesium; Magnesium Compounds; Male; Middle Aged; Oxalates; Phosphates; Proteus mirabilis; Struvite

Topics: Adult; Calcium; Child; Crystallization; Crystallography; Epithelium; Humans; Kidney; Kidney Calculi; Mucoproteins; Oxalates; Solubility

Calcium and oxalate were studied in daily, fasting and postprandial urine specimens from healthy subjects and patients with idiopathic renal calcium stones in response to a test meal free of oxalate, and supplemented with calcium and 14carbon-oxalic acid. The data showed that the amount of oxalate in fasting urine of patients with stones did not differ from that in controls. Generally, patients with stones had considerable postprandial hyperoxaluria in terms of excretion and concentration, associated with a significantly higher degree of supersaturation with regard to calcium oxalate compared to controls. These findings were paralleled by decreased intestinal absorption of 14carbon-oxalate and by unchanged 24-hour urinary oxalate. Although the source of increased postprandial oxalate in patients with stones is not clear the possibility of enhanced de novo synthesis from oxalate precursors is discussed. In patients with different types of calciuria the 2 main risk factors (hyperoxaluria and hypercalciuria) for the process of stone formation are recognizable more readily in the postprandial urine specimens than in fasting or daily urine specimens.

Topics: Adult; Aged; Calcium Oxalate; Carbon Radioisotopes; Eating; Fasting; Female; Food; Humans; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Time Factors

The high incidence of a family history and the observation of abnormally high intestinal absorption and urinary excretion of oxalate suggest to consider idiopathic calcium oxalate nephrolithiasis as a metabolic disease characterized by a disorder in oxalate transport. To test this hypothesis, the flux of 14C Oxalate through the membrane of red blood cells was investigated in 24 calcium oxalate stone formers; 18 of the 24 "idiopathic" calcium oxalate stone formers showed an increased oxalate self exchange (75%). Our data seem to support the possibility that "idiopathic" calcium oxalate nephrolithiasis may be considered as a metabolic disease marked by a defect in transmembrane transport of oxalate.

Topics: Adult; Biological Transport; Calcium Oxalate; Erythrocyte Membrane; Female; Humans; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence

Calculi of pure calcium oxalate monohydroxide are hard, polish, dark brown stones, of a very tenuous crystalline structure. On the contrary, calculi of pure bihydroxide oxalate are clear irregular stones with a spiky surface. They are more friable and less hard than monohydroxide oxalate stones. Monohydroxide oxalate stones radiologically are regular and homogeneous, whereas bihydroxide oxalate stones have an irregular aspect. Monohydroxide oxalic lithiasis is less frequent than bihydroxide oxalic lithiasis. The proportion of monohydroxide lithiasis is the same in men and women whereas bihydroxide lithiasis is more frequent in men. Of a biologic point of view, in monohydroxide lithiasis, calciuria and oxaluria are often normal while proportion of hypercalciuria and hyperoxaluria is more important in bihydroxide lithiasis. Evolutivity is clearly inferior in monohydroxide lithiasis than in bihydroxide lithiasis.

Topics: Adult; Calcium Oxalate; Crystallization; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Radiography; Sex Factors

Usually calcium nephrolithiasis is due to "idiopathic" hypercalciuria associated with failure of the compensatory mechanisms (dissolving substances and crystallisation inhibitors. Classically a sufficient diuresis, a low calcium diet, the phosphate ion or (and) the thiazidic diuretics manage to reduce the hypercalciuria and to decrease the chances of relapse. This aim may be differently reached when hyperuricosuria is associated with hypercalciuria. The use of uric acid synthesis inhibitors (allopurinol, thiopurinol) brings the frequency of the recurring stone formation down and... the calciuria often. Series dealing with 141 calcium lithiasis with hyperuricosuria.

Topics: Allopurinol; Calcium; Humans; Kidney Calculi; Oxalates; Uric Acid; Uricosuric Agents

From 3000 urinary calculi analysis, a morphological classification allowed us to appoint 7 structural types of oxalate stones, dependent on whewellite or/and weddellite. We observed evidence for correlations between biological data and these structural types, mainly between types I and hyperoxaluria, types II and hypercalciuria, types II + IV or IV and hyperparathyroïdism, as well as between whewellite and hyperuricuria. We determined in vitro calcium and oxalate concentrations ranges to crystallize various hydrate forms of calcium oxalate and we observed that whewellite form is almost the only one fitted for crystallizing in renal papilla. From this various data, it results that, in vivo, whewellite is dependent on oxalate concentration whereas weddellite is rather dependent on calcium concentration. Otherwise, differences in occurrence of morphological types of oxalate calculi were observed as a function of the patient' sex, the urinary tract localisation of calculi, or the crystalluria.

Topics: Calcium; Calcium Oxalate; Crystallization; Humans; Hyperparathyroidism; Kidney Calculi; Kidney Medulla; Oxalates; Uric Acid

The purpose of this study was to determine and to compare the frequency of hypercalciuria, hyperoxaluria and hyperuricosuria in 49 patients with a pure or mixed calcium oxalate urolithiasis. During this study, all patients were on a normal diet and had no special disease or medication. We noted that hypercalciuria (35%) and hyperoxaluria (24%) were more often associated (18%) than isolated (8 and 2%). They were more frequent in mixed stones (44% et 39%) than in pure one (29% and 16%). Hyperuricuria (39%) had a same frequency wathever the renal stone type may be. A same frequency was noted when hyperuricuria was associated with hypercalciuria and hyperoxaluria (12%) or isolated (14%). None of these three biologic disturbances was observed in 45% of our patients.

Topics: Adult; Calcium; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Risk; Uric Acid

Topics: Calcium; Citrates; Humans; Kidney; Kidney Calculi; Oxalates; Uric Acid

Analysis for calcium, magnesium, phosphorus, oxalate, uric acid, and creatinine in 24-h urine collections is often needed for the differential diagnosis of patients with renal calculi. Considerable attention has been given to improving the methods of analysis, but improper sample collection and processing can cause significant errors for calcium and oxalate in urine samples not treated with acid and for uric acid in urine samples not treated with base. The errors are related to the concentration of the analyte, the interval the sample is stored before analysis, and the original pH of the urine sample. We describe here a system of sequential acidification (to pH 1.5) and alkalinization (to pH 9) of 24-h urine samples, followed by heating at 56 degrees C for 10 min. This procedure allows accurate analysis for all the above analytes in the same 24-h collection of urine. We validated the sample-treatment protocol for 80 24-h urine collections.

Topics: Calcium; Creatinine; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Oxalates; Oxalic Acid; Phosphorus; Specimen Handling; Temperature; Time Factors; Uric Acid; Urine

Renal tubular acidosis (RTA) is a well-known metabolic disturbance that may promote recurrent renal stone formation. However, its incidence, screening criteria and association with other lithogenic metabolic abnormalities are not established in recurrent nephrolithiasis. 10 of 50 consecutive recurrent renal stone formers had a persistent fasting morning urinary pH above 6.0 and/or a basal plasma bicarbonate concentration below 20.0 mM. Acid and alkaline loads disclosed RTA in 3 patients: 1 patient had incomplete type-1 distal RTA in addition to hyperoxaluria; a second patient showed complete type-2 proximal RTA, hyperoxaluria and renal hypercaliuria; and a third patient had incomplete proximal RTA without any other metabolic derangement. These results reinforce the importance of RTA as an isolated metabolic abnormality among recurrent renal stone formers. In addition, RTA appears to be more commonly associated with other lithogenic metabolic derangements than has been previously suspected. The extensive metabolic protocol used in this study provides a useful tool in the diagnosis and therapeutic considerations of recurrent nephrolithiasis.

Topics: Acidosis, Renal Tubular; Bicarbonates; Calcium; Creatinine; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Phosphorus; Recurrence; Uric Acid

A comparative epidemiological study was done on renal lithiasis in gypsies and nongypsies in Eastern Andalucía, Spain. A family history of lithiasis in gypsies was obtained 2 to 3 times less often compared to nongypsies (1.14 versus 4.34 per cent). The male-to-female ratio of gypsies with lithiasis was 0.59 per cent compared to 1.54 per cent in others. The inverse ratio in gypsies contrasted with those obtained by various authors in western countries of white and black populations. There was a predominance of immediate family history of lithiasis in gypsies with stones (p less than 0.001, 11.81 per cent), which was not observed among nongypsies (p equals 0.80). The incidence of consanguineous marriage among gypsies was high (26.95 per cent) compared to others (4.07 per cent). There was a dependent relationship in gypsies between family history of lithiasis and consumption of meat products (p equals 0.001), dairy products and food rich in oxalic acid (p equals 0.05). In nongypsies these differences were less significant statistically and were nonexistent in the incidence of consumption of food containing oxalic acid. We ascribe the difference in the incidence of lithiasis between gypsies and other subjects principally to hereditary and dietary factors.

Topics: Adolescent; Adult; Aged; Child; Dairy Products; Diet; Ethnicity; Female; Humans; Kidney Calculi; Male; Meat; Middle Aged; Oxalates; Recurrence; Roma; Spain

Topics: Diet, Reducing; Humans; Ileum; Jejunum; Kidney Calculi; Oxalates; Postoperative Complications

Topics: Blood Glucose; Body Weight; Calcium; Female; Glucose; Humans; Kidney Calculi; Oxalates; Prognosis; Recurrence; Risk; Sodium; Uric Acid

Topics: Calcium; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Oxalates; Recurrence; Risk

Topics: Adolescent; Adult; Calcium; Calcium Oxalate; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

During 5 years, between 1978 and 1982, 40 patients (22 male, 18 female) aged 1 to 17 years presented with kidney stones at the Erlangen University Children's Hospital. Stone analysis showed calcium oxalate in 61%, calcium phosphate respectively magnesiumammonium phosphate in 33% and cystine in 6%. Calcium phosphate/ magnesiumammonium phosphate stone bearers were most frequently found in the first 5 years of age and showed more often urinary tract malformations, staghorn renal calculi, urinary tract infections and a higher urinary pH. Calcium oxalate stone bearers were more frequently found in patients of school age and had more often relatives with nephrolithiasis. In the group of calcium oxalate stones hypercalciuria, hyperoxaluria and hyperuricosuria were most frequently observed.

Topics: Adolescent; Calcium; Child; Child, Preschool; Cystinuria; Diagnosis, Differential; Female; Humans; Hydrogen-Ion Concentration; Infant; Kidney Calculi; Magnesium; Male; Oxalates; Oxalic Acid

Ionic calcium, calcium binding sites, and other urinary variables were measured in 58 patients with idiopathic calcium nephrolithiasis and 36 normal subjects. The patients showed higher urinary concentrations of calcium. The mean calcium excretion (mmole/24 hr) was 4.45 +/- 0.56 (+/- 1 SEM) in patients and 2.19 +/- 0.22 (+/- 1 SEM) in normal subjects. This difference was highly significant (P less than 0.001). The mean ionic calcium excretion (mmole/24 hr) was 1.90 +/- 0.21 (+/- 1 SEM) for patients and 0.97 +/- 0.12 (+/- 1 SEM) for control subjects. The normal subjects showed significantly higher (P less than 0.01) concentrations and total excretions of magnesium and citrate. Excretory patterns for sodium, potassium, phosphate, and oxalate were not significantly different. The normal subjects had higher mean urinary concentrations of binding sites for calcium ions (23.2 +/- 4.8 mM) than the patients (18.5 +/- 2.9 mM). However, as the patients had higher urinary volumes the difference in the 24-hr excretion of calcium binding sites was not significant statistically. Out of 58 patients 43 (74%) were hypercalciuric. Twenty patients (46%) were categorized as an absorptive group and one patient as a resorptive type, and for the rest of the patients (51%) the mechanism of hypercalciuria remained unidentified. Only two of the control subjects (5%) were found to be hypercalciuric under calcium restricted diet conditions. Though these "control" subjects excreted a high amount of calcium there was no associated increase in the fraction of the calcium in the ionic form (0.37). Patients, however, still had relatively high fractions of ionic calcium (0.48 +/- 0.03).

Topics: Calcium; Cations; Citrates; Cyclic AMP; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Sodium

Urinary excretion of the most widely studied renal stone promoting (calcium, oxalate, uric acid and phosphate) and inhibiting (citrate, magnesium, pyrophosphate and glycosaminoglycans) factors, as well as the Tamm-Horsfall mucoprotein, was evaluated in 14 children with idiopathic calcium nephrolithiasis, 6 children with renal stone disease secondary to excretory malformations and 19 normal controls. No statistically significant differences in urinary excretion of promoting and inhibiting factors were found in children with idiopathic calcium nephrolithiasis but the relationship between promoting and inhibiting factors was changed as shown by an abnormal ratio of oxalate/citrate X glycosaminoglycans. This finding suggests that there is an imbalance between promoting and inhibiting factors in children with idiopathic calcium nephrolithiasis, and it is not detected by assay of each single substance.

Topics: Adolescent; Calcium; Child; Child, Preschool; Citrates; Diphosphates; Female; Glycosaminoglycans; Humans; Kidney Calculi; Magnesium; Male; Mucoproteins; Oxalates; Phosphates; Quaternary Ammonium Compounds; Sodium; Uric Acid; Uromodulin

We describe a sensitive, simple technique for determining urinary oxalate. Urine, diluted as necessary with distilled water, is injected into an ion chromatograph. Oxalate is detected conductimetrically as a distinct peak near the tail of the chromatogram. This peak specifically represents oxalate, because it is abolished if the sample is treated with oxalate decarboxylase. We have used this technique to measure oxalate in more than 3000 consecutively received urine samples. It has a CV of 6%.

Topics: Carbonic Acid; Carboxy-Lyases; Chromatography, Ion Exchange; Humans; Immunoenzyme Techniques; Intestinal Diseases; Kidney Calculi; Oxalates; Spectrophotometry, Atomic

Two patients with documented primary hyperoxaluria have received renal allografts with successful function for 10 years and 25 months. The patient in case 1 required a ureterolithotomy 6 years post-transplantation to remove a renal calculus of calcium oxalate. This case illustrates that despite recurrence of oxalate stones in the allograft, satisfactory renal function can be maintained by careful follow-up and appropriate interventions. Factors that may be important in successful graft function include the occurrence of acute rejection episodes, avoidance of ischemic graft damage, trials of pyridoxine therapy to decrease oxalate excretion, and frequent evaluation with appropriate interventions as necessary. Renal transplantation is a suitable and possibly the preferred form of therapy of end stage renal disease in patients with primary hyperoxaluria.

Topics: Adult; Biopsy; Female; Follow-Up Studies; Graft Survival; Humans; Kidney; Kidney Calculi; Kidney Failure, Chronic; Kidney Transplantation; Oxalates; Oxalic Acid; Pyridoxine; Recurrence; Time Factors

Increasing attention is being given to oxalate as a risk factor in urinary calcium stone disease. The accuracy of some methods for measuring urine oxalate is uncertain. Using gas chromatography urine oxalate levels were 0.36 +/- 0.02 and 0.31 +/- 0.02 (mmol/24 h +/- 1 SEM) for men and women respectively of a reference population. In recurrent stone formers urinary oxalate was 0.43 +/- 0.03 in males and 0.38 +/- 0.04 for females whilst solitary stone forming females excreted only 0.31 +/- 0.04 mmol/24 h. The difference between males and females of the reference population was significant (p less than 0.05) as was the difference between reference males and male stone formers.

Topics: Adolescent; Adult; Aged; Female; Humans; Kidney Calculi; Male; Middle Aged; New Zealand; Oxalates; Sex Factors

Hyperoxaluria, alone or associated with hypercalciuria, has been detected in 69 of 450 patients with recurrent stones (15.3 per cent). The 3 main findings associated with hyperoxaluria were 1) oxalate hyperabsorption, 2) hyperoxalemia and 3) increased or decreased oxalate clearance. Correction of oxalate hyperabsorption by administration of diethylaminoethanol cellulose showed good results through a 5-year followup. Succinimide, given to the hyperoxalemic group, and a combination of phosphate and magnesium, given to the group with altered clearances, showed poorer results.

Topics: Adult; Calcium Oxalate; Cellulose; DEAE-Cellulose; Humans; Intestinal Absorption; Kidney Calculi; Magnesium; Magnesium Chloride; Oxalates; Phosphates; Recurrence; Succinimides; Time Factors

We studied the effect of bendroflumethiazide on a risk factor index, COSP, reflecting the stone-forming potential of urinary calcium oxalate. This index includes the concentrations of three stone promotors: calcium, oxalate, and uric acid in its numerator, and two stone inhibitors: magnesium and citrate, in its denominator. These risk factors were measured in 4-hour and 24-hour urinary specimens obtained under fixed conditions of food and fluid intake. Eight normal males were studied before and after two and four weeks of continued thiazide treatment. Thiazide 2.5 mg b.i.d. was given for two weeks, followed by 2.5 mg t.i.d. for another two weeks. Before treatment COSP exhibited a pronounced diurnal variation with peaks between 8 a.m. and noon, and 8 p.m. and midnight. After four weeks of thiazide treatment suppression of two stone promotors, calcium (p less than 0.01) and uric acid (p less than 0.02), and reduced COSP by 36 to 95% in each subject (median: -71%, p less than 0.01). Moreover, thiazide abolished the diurnal variation of COSP. After the initial two weeks of thiazide 2.5 mg b.i.d., almost identical effects were observed. Nearly all the changes in COSP were explained by the effects on urinary calcium. This marked suppression of COSP supports the theory that thiazides may be useful in the prevention of renal calcium oxalate stone formation.

Topics: Adult; Bendroflumethiazide; Calcium; Calcium Oxalate; Humans; Kidney Calculi; Male; Oxalates; Risk; Uric Acid

Topics: Allopurinol; Calcium Oxalate; Calcium, Dietary; Cellulose; Citrates; Citric Acid; Combined Modality Therapy; Fluid Therapy; Humans; Hydrochlorothiazide; Kidney Calculi; Magnesium; Oxalates; Phosphates; Urinary Calculi

In 12 patients with idiopathic calcium oxalate calculi pyridoxine was administered. Within six weeks mean daily oxalic acid excretion decreased from 480 +/- 122 mumol to 336 +/- 83 mumol. Glycolic acid excretion fell from 208 +/- 51 mumol to 153 +/- 26 mumol (normal range: oxalic acid 228-412 mumol/day, glycolic acid 130-290 mumol/day). The reduction of oxalic acid excretion seems to be beneficial in prevention of idiopathic calcium oxalate calculi.

Topics: Calcium Oxalate; Glycolates; Humans; Kidney Calculi; Oxalates; Oxalic Acid; Pyridoxine

In 30 calcium stone formers urinary citrate, magnesium, calcium, phosphorus, uric acid and oxalate excretion were compared with the activity product ratios and formation product ratios of oxalate, brushite and monosodium urate. A positive correlation was found between calcium and phosphorus excretions and APRox and APRbr; no correlation was found between oxalate, uric acid, citrate and magnesium excretion and APR or FPR. Thus calcium and phosphorus contribute significantly to the increments of urine saturation; citrate and magnesium do not modify the inhibitor urinary activity, and oxalate and uric acid do not influence inhibition and saturation activities of urine.

Topics: Adolescent; Adult; Aged; Calcium; Calcium Phosphates; Humans; Kidney Calculi; Middle Aged; Oxalates; Oxalic Acid; Phosphorus; Uric Acid

A case of oxalate lithiasis associated with Abetalipoproteinemia is reported. The excessive absorption of dietary oxalate in this patient with fat malabsorption occurs because unabsorbed fatty acids in the bowel lumen combine with calcium ions which would otherwise impair oxalate absorption by forming insoluble calcium oxalate crystals. The medical management include dietary fat restriction and supplements of the fat soluble vitamins A, E and K. The prognostic is poor particularly in the neurological and retinal component of this disease.

Topics: Abetalipoproteinemia; Adolescent; Humans; Kidney Calculi; Male; Oxalates

This discussion was selected from the weekly Grand Rounds in the Department of Medicine, University of Washington, Seattle. Taken from the transcription, it has been edited by Drs Paul G. Ramsey, Assistant Professor of Medicine, and Philip J. Fialkow, Professor of Medicine and Chairman of the Department of Medicine.

Topics: Acidosis, Renal Tubular; Calcitriol; Calcium; Cystinuria; Humans; Kidney Calculi; Oxalates; Uric Acid

The urinary citrate excretion was examined in patients with nephrolithiasis who were categorized on the basis of different physiologic or metabolic abnormalities. A wide prevalence of low citrate excretion (hypocitraturia) was observed, with over one half of our patients with stones exhibiting it. Hypocitraturia was found in all patient categories except primary hyperparathyroidism and hyperuricosuric calcium oxalate nephrolithiasis. As expected, hypocitraturia was present in renal tubular acidosis and in enteric hyperoxaluria. However, urinary citrate was also low in absorptive and renal hypercalciurias, and in patients in whom an acid-base disturbance was clearly excluded.

Topics: Acidosis, Renal Tubular; Adult; Calcium; Citrates; Citric Acid; Female; Humans; Kidney; Kidney Calculi; Male; Menopause; Middle Aged; Oxalates; Sex Factors

Topics: Child, Preschool; Female; Fractures, Spontaneous; Growth Disorders; Humans; Hypercalcemia; Kidney Calculi; Kidney Failure, Chronic; Metabolism, Inborn Errors; Oxalates; Oxalic Acid

The analysis of renal calculi is an oft-neglected corner of clinical biochemistry. This study compares results obtained by the conventional qualitative methods with results from quantitative and infrared methods and also investigates the role of x-ray diffraction analysis. Infrared spectroscopy, using a KBr disc technique, was found to be the single most useful method, being fast, simple to learn, using little sample, and in general permitting positive identification of most of the components found in renal calculi. A major advantage is that this method has approximately equal sensitivity for oxalate and phosphate, unlike the wet chemical methods. Infrared analysis is also useful in identifying the spurious materials sometimes submitted as renal calculi. X-ray diffraction analysis is not a technique that is routinely available, but it does provide information not given by other methods, eg, distinguishing Ca(COO)2 . H2O from Ca(COO)2 . 2H2O. For complete analysis a combination of methods was adopted; carbonate is tested for using a microchemical technique, calcium, magnesium, and phosphate are quantitated by routine methods, and infrared analysis is used to detect oxalate and organic components. It must be emphasised that any method is only as good as the sample used, and different areas of the calculus must be analysed separately if useful results are to be obtained.

Topics: Carbonates; Cystine; Humans; Kidney Calculi; Magnesium; Oxalates; Phosphates; Quaternary Ammonium Compounds; Spectrophotometry, Infrared; Uric Acid; X-Ray Diffraction

Topics: Calcium; DEAE-Cellulose; Humans; Kidney Calculi; Magnesium; Magnesium Compounds; Oxalates; Phosphates; Succinimides

Urinary citrate excretion was measured with a specific enzymatic technique in normal subjects and in an unselected group of patients with recurrent calcium oxalate stones. Hypocitraturia (citrate levels less than those present in 95 per cent of the normal population) was detected in 7 of 46 patients with stones (15 per cent). Hypocitraturia was the only metabolic abnormality in 6 patients.

Topics: Adult; Calcium; Calcium Oxalate; Citrates; Citric Acid; Creatinine; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Sex Factors

The circadian (circannual for oxalic acid) variations of 13 urinary variables (volume, creatinine, calcium, oxalic acid, glycolic acid, 17-ketosteroids, 17-hydroxycorticosteroids, phosphates, urea, uric acid, chloride, sodium, and potassium) have been documented in 7 calcium oxalate renal stone formers and 7 healthy men (control group). Urine was collected every 4 h over a period of 24 h. All subjects had the same synchronization: diurnal activity from 07(00) to 23(00) +/- 1 h and nocturnal rest; meals were given at fixed clock hours (08(00), 12(30) and 20(00) +/- 1 h). A statistically-significant rhythm (p less than 0.05) was validated for all variables except urea and calcium in healthy men. In renal stone formers, 6 variables (calcium, oxalic acid, and glycolic acid in particular) had no detectable circadian rhythm. However, a periodicity of c. 8 h (ultradian rhythm) was demonstrated for calcium and oxalic acid with peaks being located around 02(00), 10(00), and 18(00). No circannual variations in oxalic acid output could be observed. The present study shows an alteration of the periodicity of calcium and oxalic metabolisms, i.e. the loss of a circadian (24-h) rhythm and the occurrence of an ultradian rhythm of 8 h. The risk of calcium-oxalate crystallisation appears thus greater at 02(00), 10(00), and 18(00). Furthermore, any study dealing with oxalic acid excretion should state the season of urine collection when comparing renal stone formers and healthy subjects, as significant differences in oxaluria may appear during the summer months and not during the rest of the year.

Topics: Adult; Calcium; Calcium Oxalate; Circadian Rhythm; Glycolates; Humans; Kidney Calculi; Oxalates; Seasons

Topics: Adolescent; Bone Diseases; Femur; Humans; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Radiography; Renal Dialysis; Sclerosis

To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria. We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.

Topics: Adult; Calcium; Calcium, Dietary; Female; Humans; Intestinal Absorption; Kidney; Kidney Calculi; Male; Oxalates; Oxalic Acid; Risk

In an effort to develop a simple and reliable method with which to assess the propensity for spontaneous nucleation of calcium oxalate and brushite in urine, the permissible increment of oxalate and calcium was calculated. This represented the additional amount of oxalate or calcium that could be added to urine in three hours before spontaneous precipitation of calcium oxalate or brushite was initiated. The permissible increment of oxalate inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of calcium oxalate, which was previously shown to reflect a quantitative measure of the likelihood for spontaneous nucleation. Similarly, the permissible increment of calcium inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of brushite. The permissible increments in oxalate and calcium were significantly lower (P less than 0.001) in patients with renal stones than in control subjects. Moreover, treatment with thiazides, allopurinol, sodium cellulose phosphate, orthophosphate, and diphosphonate significantly raised the permissible increment of oxalate in patients with stones. Thus, the permissible increment was reliable in discriminating "stone-forming" from control urine and in assessing response to treatment.

Topics: Calcium; Calcium Oxalate; Calcium Phosphates; Crystallization; Humans; Kidney Calculi; Mathematics; Oxalates; Oxalic Acid

Topics: Adult; Female; Follow-Up Studies; Humans; Kidney Calculi; Male; Oxalates

Urinary excretion of oxalate, calcium and urate has been investigated in 88 patients affected by idiopathic calcium oxalate stone disease and in 20 normal subjects. Of these ions, only oxalate was found significantly higher in stone formers. Defining hyperoxaluria as urinary oxalate excretion greater than 2 SD above normal, 50% of stone-forming people were found to be hyperoxaluric. When stone formers were classified in normo- and hyperoxaluric, the prevalence of hypercalciuria, hyperuricuria, family history of stone disease and recurrencies in stone formation was the same in both groups. It is concluded that hyperoxaluria is a frequent finding in finding in idiopathic calcium oxalate renal stone disease.

Topics: Adult; Calcium; Calcium Oxalate; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence; Uric Acid

Three hundred and ninety-two stone formers were investigated to exclude systemic disorders and to define the presence of haematological and urinary abnormality commonly associated with stone disease. Increased urinary excretion of calcium, oxalate or uric acid was found in 40% and there was more than one abnormality in 16% of the patients. The dietary habit of stone formers did not differ significantly from that of control subjects. Dietary advice to increase the consumption of fibre and reduce the consumption of sugar, refined carbohydrates and animal protein produced a significant reduction in the urinary excretion of calcium, oxalate and uric acid. We consider that reduction of the nutrient density of the diet by this means is the first line of management of idiopathic stone formers.

Topics: Adolescent; Adult; Aged; Calcium; Child; Dietary Carbohydrates; Dietary Fiber; Dietary Proteins; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Patient Compliance; Risk; Uric Acid

Topics: Calcium Oxalate; Humans; Kidney Calculi; Oxalates; Pyridoxine; Recurrence

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.

Topics: Animals; Calcium Oxalate; Crystallization; Ethylene Glycols; Kidney Calculi; Kidney Tubules; Magnesium Deficiency; Male; Microscopy, Electron, Scanning; Oxalates; Oxalic Acid; Rats; Rats, Inbred Strains

The pathophysiology of various metabolic and other medical disorders that may complicate Crohn's disease is outlined. Measures that may help to prevent or mitigate these complications are discussed.

Topics: Bile Acids and Salts; Crohn Disease; Humans; Intestinal Absorption; Iron Deficiencies; Kidney Calculi; Metabolic Diseases; Oxalates; Vitamin B 12; Zinc

1. The renal clearance of [14C]oxalate was assessed by the constant-infusion technique and single-injection technique (plasma sampling only: one-compartment and two-compartment model; plasma and urine sampling). Healthy volunteers and patients with renal stones were studied. 2. Results with the constant-infusion techniques (with and without urine sampling) were not significantly different from each other. 3. The renal clearance of [14C]oxalate measured with the single-injection technique as compared with the constant-infusion technique was overestimated in the single-injection one-compartment model (52%) as well as in the two-compartment model (30%). 4. The calculated level of plasma oxalate in the healthy volunteers ranged from 1.04 to 1.78 mumol/l (mean 1.39). 5. The biological half-life of [14C]oxalate, estimated by the cumulative excretion of 14C in urine after equilibrium had been established, was 128 min (range: 113-142). 6. The oxalate/creatinine clearance ratio in the healthy volunteers ranged from 1.73 to 2.22 (mean 2.01).

Topics: Female; Half-Life; Humans; Infusions, Parenteral; Injections, Intravenous; Kidney; Kidney Calculi; Male; Metabolic Clearance Rate; Oxalates; Oxalic Acid

1. Seventeen healthy controls and 63 patients with idiopathic calcium stone disease of the urinary tract were investigated for urinary calcium and oxalate excretion and for [14C]oxalate intestinal absorption. 2. Under comparable controlled dietary intake a significant increase in calcium excretion as found in patients with stone disease. Oxalate excretion and [14C]oxalate intestinal absorption were mildly but not significantly increased. When patients with stone disease were subdivided into normocalciuric and hypercalciuric subjects, oxalate excretion and [14C]oxalate absorption were significantly increased in the latter. There was a significant direct relationship between calcium excretion and both oxalate excretion and [14C]oxalate absorption. 3. [14C]Oxalate absorption increased significantly in 22 stone-formers when dietary calcium was changed from normal to low. 4. The kinetics of [14C]oxalate intestinal absorption showed that the main difference between normocalciuric and hypercalciuric subjects occurred within the first 6 h after the oxalate-labelled meal. 5. These results confirm that mild hyperoxaluria is a frequent feature of idiopathic calcium stone disease even when patients and controls are studied under controlled dietary conditions. Our data are consistent with the hypothesis that hyperoxaluria is secondary to calcium hyperabsorption and is upper intestinal in origin.

Topics: Adult; Calcium; Female; Humans; Intestinal Absorption; Kidney Calculi; Kinetics; Male; Oxalates; Oxalic Acid

Topics: Adult; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

Seasonal variations in urinary calcium and oxalate excretion, serum 25(OH)D3 and albumin level were studied in 11 normo- and 11 hypercalciuric renal stone-formers, in 10 healthy subjects and in 14 long-stay hospital patients during one year. Serum albumin levels increased significantly during May--October in all four groups, whereas no significant changes occurred in serum calcium values when adjusted for differences in serum albumin concentration. Serum 25(OH)D3 level, urinary calcium and oxalate excretion were significantly higher during May--October than November--April in all except the long-stay hospital patients, whose corresponding values showed no seasonal changes and whose serum 25(OH)D3 levels as well as urinary calcium excretion were significantly lower than in the other three groups. The serum 25(OH)D3 level was significantly higher throughout the year in hypercalciuric than normocalciuric stone-formers. The hypercalciuric patients also passed more stones than the normocalciuric patients during a period of 9 years. There was a positive correlation between serum 25(OH)D3 and urinary calcium, between serum 25(OH)D3 and stone episodes and between urinary calcium and stone episodes. Because of this positive correlation, it might be useful to concentrate preventive therapy for recurrent renal stones to the light period only.

Topics: Adult; Calcium; Dihydroxycholecalciferols; Female; Finland; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Seasons; Serum Albumin

The importance of diet within the framework of effective therapeutic measures in the prophylaxis of recurring lithiasis is emphasised. Some diet sheets are presented.

Topics: Calcium; Cystine; Diet Therapy; Humans; Intestinal Absorption; Kidney Calculi; Oxalates; Uric Acid

We report on our experience with 9 cystine-lithiasis patients who were treated with large doses of ascorbic acid (5 g/day) for periods ranging from 6-27 months. We observed recidive lithogenesis in only 3 patients during this time. The influence of ascorbic acid on the excretion of cystine and oxalate in the urine is discussed. A lack of side effects and the significantly lower frequency of recidivation justify the further use of ascorbic as an alternative medication in cystine lithiasis.

Topics: Adult; Ascorbic Acid; Cystine; Cystinuria; Dose-Response Relationship, Drug; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Oxalic Acid; Recurrence; Urinary Bladder Calculi; Urinary Calculi

Urinary excretion rate of oxalate was measured in 79 patients with idiopathic calcium (Ca) nephrolithiasis and the results were compared with those obtained in 28 healthy volunteers. The group of stone formers consisted of 20 patients with idiopathic hypercalciuria (IHC) of the absorptive type, 23 patients with IHC of the renal type, 11 patients with hypercalciuria secondary to dietary factors, 1 patient with hyperuricosuria (as an isolated finding) and 24 patients without hypercalciuria nor hyperuricosuria. Classification was based upon the urinary excretion rate of uric acid, as well as that of calcium measured under 3 different dietary conditions (i.e. free diet, free diet supplemented with 3 g Ca/day for 3 days, and diet free of dairy products for 5 days). On a free diet, normal values of oxaluria ranged from 125 to 435 mumol/24 h; an elevated value was observed in 11 (14%) patients, 5 of whom belonged to the subgroup without hypercalciuria nor hyperuricosuria. On a low Ca diet, mild hyperoxaluria occurred in 3 controls and in 19 patients, the tendency to develop hyperoxaluria being particularly marked in the subgroup with absorptive-IHC. Moreover, there was a positive correlation between oxaluria on a low Ca diet and the estimated degree of intestinal absorption of Ca. This study confirms the finding that on a free diet, the incidence of mild hyperoxaluria amongst idiopathic stone formers is rather low. It shows, however, that a significant percentage of patients classically referred to as "without metabolic disorder" have in fact slight hyperoxaluria, an observation with a potential therapeutic impact. Finally, it shows that on a low Ca diet, patients with absorptive-IHC are particularly prone to develop hyperoxaluria: the latter observation renders questionable the relevance of a low Ca diet for patients with absorptive IHC, unless their intake of oxalate is simultaneously reduced.

Topics: Adolescent; Adult; Aged; Calcium; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Uric Acid

Hyperoxaluria and kidney stones are frequent following intestinal bypass operations. The urinary oxalate excretion was studied for 10-13 days during enteral and parenteral nutrition in six patients operated on because of massive obesity with a jejunoileostomy. The oxalate excretion in urine was higher than normal in all patients on normal diet. The excretion decreased on low-oxalate diet. Further decrease was observed during total parenteral nutrition (TPN). The oxalate excretion was stabilized at a low level within 48 h after the start of TPN and was unchanged during the rest of the study. This included a period of 2 days when a load of the oxalate precursor glycine (10 and 20 g) was given parenterally to five patients, resulting in increased serum glycine concentration. A slight decrease in oxalate excretion was found when the amino acid part (Vamin with 10% glucose) of the TPN solution was given enterally instead of parenterally in two patients. This study has indicated that the main reason for hyperoxaluria in patients with intestinal bypass operations is hyperabsorption of dietary oxalate. It seems likely that these patients have a normal endogenous oxalate production.

Topics: Adult; Female; Follow-Up Studies; Humans; Hyperoxaluria; Jejunoileal Bypass; Kidney Calculi; Male; Middle Aged; Obesity, Morbid; Oxalates; Parenteral Nutrition, Total; Postoperative Period; Risk Factors; Time Factors

Topics: Allopurinol; Calcium Oxalate; Citrates; Citric Acid; Creatinine; Diphosphates; Humans; Kidney Calculi; Lactates; Lactic Acid; Oxalates; Uric Acid

Topics: Adolescent; Adult; Aged; Calcium; Child; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

The principle of isotachophoresis has been used to develop a simple, specific and sensitive analytical procedure for the determination of oxalate in unprocessed urine. Analytical conditions were optimized. The accuracy and precision of the method were estimated. The specificity was checked with oxalate decarboxylase. Separation of oxalate from a number of organic acids was achieved. The influence of factors such as storage, calcium concentration, pH or ionic strength was examined. The 24-h urine excretion rates for healthy children, healthy adults and for patients with idiopathic stone formation were established. Lower absolute excretion rates were found in children and females. Urinary oxalate/creatinine ratios were higher in children than in adults. The mean oxalate excretion in 24-h urines of adult healthy individuals was 413 +/- 150 mumol per 24 h per 1.73 m2 (range 195-732). The mean oxalate/creatinine ratio was 0.033 +/- 0.011 (range 0.018-0.065).

Topics: Adult; Calcium; Carboxy-Lyases; Child; Drug Storage; Electrophoresis; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Spectrophotometry, Ultraviolet; Zinc

Topics: Calcium; Humans; Kidney Calculi; Oxalates

Because of their amphiphilic properties, bile acids have important physiological functions. However, they can also be pathogenetically active. Some recent findings on the biochemistry and enterohepatic circulation of bile acids are presented. In contrast to the adult liver where the only primary bile acids formed are cholic- and chenodeoxycholic acid, the foetal liver is able to synthesise a variety of "atypical" bile acids. Under certain circumstances, a retrograde differentiation is possible in the adult. The very effective transport systems in gut and in the sinusoidal and canalicular membrane of the liver cell limit the bile acids almost exclusively to the enterohepatic circulation. During transport in blood, through biomembranes and in the liver cytosol, bile acids are bound to carrier proteins. The carrier has been detected using photoaffinity labelling. Following biotransformation (sulphation and glucuronidation) pathogenetically active bile acids can be converted into derivatives which can be rapidly eliminated. Disturbances of these mechanisms result in functional defects and diseases. The pathological significance of bile acids in hepato-biliary diseases is represented with regard to the cholestatic and proliferative effect of individual bile acids. The significance of bile acids in chologenic diarrhea, steatorrhea and enteral hyperoxaluria are presented as examples of the pathogenetic effects of bile acids on the gut. In these diseases it is possible to recognise the specific effects of certain bile acids on the colon mucosa. Recent studies have demonstrated that bile acids are possibly of pathogenetic significance in the case of epidemiologically proven relationship between colon carcinoma and high fat, high cholesterol and low fibre diets.

Topics: Bile Acids and Salts; Biliary Tract Diseases; Biological Transport, Active; Carrier Proteins; Celiac Disease; Cholestasis; Colonic Neoplasms; Cytosol; Diarrhea; Humans; Intestinal Absorption; Kidney Calculi; Lipoproteins, HDL; Liver; Liver Diseases; Molecular Weight; Oxalates

Topics: Animals; Calcium Carbonate; Calcium Oxalate; Crystallization; Humans; Hypocalcemia; Ileum; Intestinal Absorption; Jejunum; Kidney Calculi; Obesity; Oxalates; Rats; Surgical Procedures, Operative

Oral sodium cellulose phosphate, an inhibitor of intestinal calcium absorption, may reduce urinary magnesium, increase urinary oxalate, and have a limited hypocalciuric action or cause negative calcium balance in the absence of increased calcium absorption or in the presence of renal calcium "leak". To overcome these potential complications, we have taken the following precautions: oral magnesium supplements were given, a moderate oxalate restriction was imposed, a modest dose of sodium cellulose phosphate was used (usually 10 g per day), and only patients with documented absorptive hypercalciuria were treated. During a cumulative treatment period of 42.8 years, 18 patients with recurrent calcium nephrolithiasis showed a sustained reduction in urinary calcium, without developing consistent or substantial reduction in urinary magnesium, hyperoxaluria, hyperparathyroidism, or reduced bone density, Urinary saturation (relative saturation ratio) of calcium oxalate and brushite typically decreased. Remission of stone disease was found in 78 per cent of patients. We conclude that sodium cellulose phosphate is a useful drug for absorptive hypercalciuria when used appropriately.

Topics: Calcium; Cellulose; Female; Humans; Intestinal Absorption; Kidney Calculi; Magnesium; Malabsorption Syndromes; Male; Oxalates

A 32-year-old women was treated for overweight by gastrointestinal bypass surgery. Following surgery, repeated calcium oxalate nephrolithiasis was observed and secondary hyperoxaluria was diagnosed. Treatment with low oxalate and fat diet resulted in normal urinary oxalic acid excretion; no further stone formation was observed.

Topics: Adult; Dietary Fats; Female; Humans; Ileum; Kidney Calculi; Obesity; Oxalates; Oxalic Acid; Postoperative Complications

Topics: Aldehyde-Ketone Transferases; Calcinosis; Carbohydrate Metabolism, Inborn Errors; Child; Child, Preschool; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Glyoxylates; Humans; Ketoglutaric Acids; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Oxo-Acid-Lyases

Topics: Ammonia; Carbonates; Child; Child, Preschool; Cystine; Female; Humans; Infant; Kidney Calculi; Male; Minerals; Oxalates; Ureteral Calculi; Uric Acid; Urinary Bladder Calculi; Urinary Calculi

Renal failure secondary to oxalate interstitial nephritis developed in three patients with malabsorption and steatorrhea following a jejunoileal bypass, extensive small intestine resection and a partial gastrectomy. Hyperoxaluria was documented in two of the cases. The possibility that this complication can occur in patients after a jejunoileal bypass operation is now recognized. This report shows that it can also occur in patients with other bowel disorders that cause malabsorption and steatorrhea. Since the prognosis for patients with oxalate nephropathy is poor, renal function should be closely monitored in patients who are at risk because of these disorders. Therapy should be directed at correcting malabsorption, steatorrhea and hyperoxaluria. When the renal function of patients with a jejunoileal bypass continues to decline despite intensive medical therapy, restoration of bowel continuity is strongly recommended.

Topics: Female; Gastrectomy; Gastrointestinal Diseases; Humans; Kidney Calculi; Kidney Diseases; Kidney Tubules; Male; Middle Aged; Nephrocalcinosis; Oxalates; Postoperative Complications

This 48-year-old male developed renal insufficiency, peripheral sensitivity to cold, occasional ventricular extrasystoles and atrio-ventricular block. He died suddenly after ventricular fibrillation. Autopsy showed extensive deposits of oxalate crystals in the kidney, myocardium, arterial walls of the extremities, and in many other visceral organs. The atrio-ventricular (A-V) node was also severely involved and marked fibrosis was found in the common A-V bundle (His) and in both bundle branches. The A-V node artery showed mural crystals and the lumen was narrowed by 50 per cent. Features supporting the diagnosis of primary oxalosis with cardiac manifestations include the onset of urolithiasis at 10 years of age, and 5 other siblings all having died of "renal disease" in infancy.

Topics: Arrhythmias, Cardiac; Cardiac Complexes, Premature; Heart Block; Heart Conduction System; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Myocardium; Oxalates

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic di

Topics: Adult; Aged; Ambulatory Care; Calcium; Cyclic AMP; Female; Glomerular Filtration Rate; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Parathyroid Hormone; Uric Acid

Topics: Ascorbic Acid; Calcium Oxalate; Diet; Gastrointestinal Diseases; Glycine; Glyoxylates; Humans; Intestinal Absorption; Kidney Calculi; Oxalates

Topics: Adult; Aged; Bacterial Infections; Calcium; Child; Cystinuria; Greece; Humans; Kidney Calculi; Oxalates; Uric Acid; Urinary Tract Infections

Topics: Adolescent; Calcium; Child; Child, Preschool; Female; Humans; Kidney Calculi; Male; Oxalates

Topics: Calcium; Child; Female; Humans; Hyperparathyroidism; Kidney Calculi; Male; Oxalates; Radiography; Uric Acid

Topics: Adenosine Deaminase; Amino Acid Metabolism, Inborn Errors; B-Lymphocytes; Child; Consanguinity; Female; Humans; Immunoglobulins; Immunologic Deficiency Syndromes; Kidney Calculi; Lymphocytes; Male; Nucleoside Deaminases; Oxalates; Pedigree; Purine-Pyrimidine Metabolism, Inborn Errors; Rosette Formation; T-Lymphocytes

We induced the deposition of calcium oxalate crystals in rat kidney by intraperitoneal administration of 4-hydroxy-L-proline or sodium oxalate and studied the amounts and size distribution characteristics of the deposited crystals. Intravenous administration of sodium copper chlorophyllin inhibited the deposition and growth of calcium oxalate crystals induced by 4-hydroxy-L-proline or sodium oxalate. This finding may be of importance in calcium oxalate urolithiasis.

Topics: Animals; Calcium Oxalate; Chlorophyll; Chlorophyllides; Crystallization; Hydroxyproline; Kidney Calculi; Male; Oxalates; Rats

Effects of standard mineral, free, and low calcium--low oxalate diets on the urinary excretion of calcium and oxalate were studied in 153 consecutive patients with single or recurrent renal/ureteral stone. The patients were divided into four groups: 78 men with single stone (MS), 40 men with recurrent stone (MR), 30 women with single stone (WS), and 5 women with recurrent stone (WR). The urine volume was altered significantly (p less than 0.001) by the diet. The sex and the diet had a significant influence on the urinary excretion of calcium. The urinary excretion of oxalate was altered significantly by the diet (p less than 0.001), but not by sex nor by the number of stones. The goal for the low calcium--low oxalate diet (the simple concentration product under 26) was reached in MS and WS. The excretion of urinary calcium and oxalate increased and urine volume decreased in the samples collected at home when compared with the samples collected in the hospital. This was interpreted as a failure of the dietary regimen at home.

Topics: Adolescent; Adult; Aged; Calcium; Diet; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence; Sex Factors; Ureteral Calculi

A 54-year old man who had been taking triamterene (150 mg daily) over a period of 8 months, passed a 3 mm stone partly coated with mustard-colored substance. Metabolic evaluation showed only mild-hyperoxaluria. Through IR spectrography after microdissection, thin-layer chromatography, UV light examination, and mass spectrometry, the stone if found to consist of 70% whewellite, 5% protein, 5% carbapatite and 20% triamterene and hydroxylated triamterene, and perhaps also the sulfate conjugate of this metabolite. In spite of the few number of observations (two cases have been reported previously), triamterene seems likely to induce stone formation, both alone and associated with urate or oxalate, and triamterene should be used cautiously in patients with a predisposition for nephrolithiasis.

Topics: Humans; Hydroxylation; Kidney Calculi; Male; Middle Aged; Oxalates; Triamterene

A simple, convenient method for the analysis of renal calculi is presented. The method allows the quantitative estimation of oxalate, urate, calcium, magnesium, xanthine, and phosphate; a qualitative analysis for ammonia, carbonate, and cystine is also done. The estimations can be done with specimens of calculi as small as 1 mg. The results of analyses of some calculi from patients are presented and discussed.

Topics: Ammonia; Calcium; Carbonates; Cystine; Humans; Kidney Calculi; Magnesium; Methods; Oxalates; Phosphates; Uric Acid; Xanthines

On the basis of what we know about urinary supersaturation and particle growth inhibitors stone formation is unlikely to start from free crystalluric particles in the renal tubule. Therefore, the object of this study is to report data on the intrarenal distribution of calcium and oxalate in man and to examine a possible relationship between calcium and oxalate concentrations in the renal tissue and stone formation. Fresh human renal tissue was obtained at operation from 7 subjects. The calcium concentrations in the papilla, medulla and cortex were measured by atomic absorption spectrophotometry. A radioenzymatic procedure was used to determine the corresponding oxalate concentrations. Significantly higher concentrations of calcium and oxalate were observed in the papilla compared to the medulla. The medulla, in turn, contained higher concentrations than the cortex. Calcium and oxalate concentrations were 6 and 25 times higher in the normal papilla than in the urine, respectively. The ion product of calcium oxalate concentrations in the human renal tissue have not been investigated, although the frequent finding of calcification in the renal papilla suggests that they may exist. The observed intrarenal calcium and oxalate concentration gradients seem to be a significant mechanism in the pathogenesis of papillary calcification and a strong indication for renal stone formation to start from fixed crystalluric particles in the papilla.

Topics: Calcium; Humans; Kidney; Kidney Calculi; Kidney Cortex; Kidney Medulla; Oxalates

Urinary oxalate was determined in an ambulatory setting in 107 patients with an increased intestinal calcium absorption rate in whom stones formed, 34 patients with normal calcium absorption in whom stones formed and 34 control subjects without stones. Urinary oxalate excretion was not significantly different when the diet was changed from a random to a calcium-restricted diet. Moreover, urinary oxalate was not higher during summer months when intestinal calcium absorption may have been stimulated. Diet history disclosed that many patients with an increased calcium absorption rate had been on a moderate oxalate-restricted diet, often as part of a calcium-restricted regimen for the control of hypercalciuria. The results indicate that renal oxalate excretion in an ambulatory setting is not critically dependent on the state of calcium absorption and intake, and that the imposition of a low calcium dietary regimen in patients with an increased calcium absorption and in whom stones form does not necessarily augment oxalate excretion.

Topics: Adult; Calcium; Calcium, Dietary; Diet; Female; Humans; Intestinal Absorption; Kidney; Kidney Calculi; Male; Oxalates; Seasons

Topics: Adolescent; Apatites; Child; Child, Preschool; Cystine; Female; Humans; Infant; Infant, Newborn; Kidney Calculi; Male; Oxalates; Phosphoranes; Radiography; Ureteral Calculi; Uric Acid; Xanthines

Thirty-four male and seven female patients with urolithiasis were treated with 300 mg allopurinol daily for one year in order to prevent stone recurrences. The mean serum-urate concentration in all patients, and the urine urate excretion in patients with a pre-treatment urate excretion above 250 mmol per mol creatinine were significantly reduced. The mean urinary excretion of calcium, magnesium and oxalate was unaffected by the treatment, although six of eight patients with a pre-treatment oxalate excretion above 25 mmol per mol creatinine demonstrated lower urine oxalate values during the treatment. No significant differences were obtained concerning the calcium/magnesium or calcium x oxalate/magnesium x creatinine quotients, but lower values of the calcium x oxalate x urate/magnesium x creatinine2 quotient were observed during allopurinol administration.

Topics: Allopurinol; Calcium; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Recurrence; Uric Acid; Urine

The authors report the association, in a 64-year old man with previous large ileal resection (110 cm) for Crohn's disease, of gallstone and oxalate renal stones. The oxaluria was 60 mg per day (normal, less than 25 mg) and the fecal fat excretion was 50 g per day (normal, less than 6 g). A low--oxalate and--fat diet for 3 months reduced dramatically the steatorrhea, but was totally ineffective for the reduction of hyperoxaluria. The physiopathological mechanisms and the therapeutic consequences of these metabolic complications of ileal resections are discussed.

Topics: Celiac Disease; Cholelithiasis; Crohn Disease; Humans; Ileum; Kidney Calculi; Male; Middle Aged; Oxalates; Postoperative Complications

We measured serum and urinary citrate, oxalate, calcium, and magnesium in 22 normal subjects and in 16 patients with malabsorption. The patients had subnormal levels of serum citrate and magnesium during fasting, subnormal 24-hour levels of urinary citrate, magnesium, and calcium, and excessive levels of urinary oxalate. Daily citrate excretion averaged only 15 per cent of normal. The hypocitraturia in the patients resulted from a subnormal filtered load of citrate and abnormally high net tubular reabsorption of the anion. An oral citrate supplement raised both the serum concentration and the filtered load of citrate to normal fasting values, but net tubular reabsorption remained abnormally high and urinary excretion abnormally low. Intramuscular magnesium sulfate, which corrected the hypomagnesemia and hypomagnesuria, had no effect on serum citrate or its filtered load. Nevertheless the injection restored net tubular reabsorption of citrate to normal and partially improved the hypocitraturia. Full correction of the hypocitraturia was achieved by combined treatment with oral citrate and intramuscular magnesium sulfate. Hypocitraturia may contribute to the formation of oxalate stones in these patients, and therefore our treatment may help to prevent this complication.

Topics: Administration, Oral; Adult; Calcium; Citrates; Female; Humans; Injections, Intramuscular; Kidney; Kidney Calculi; Kidney Tubules; Magnesium; Magnesium Sulfate; Malabsorption Syndromes; Male; Middle Aged; Oxalates

In summary it can be stated that clinically and radiologically, nephrolithiasis und nephrocalcinosis are not uncommonly encountered together. It is the aim of x-ray diagnostic to detect stones and parenchymal calcification, to assess localisation, size and numer or extent, to recognise secondary changes in the renal parenchyma and urinary-tract resulting from stones and to aid the search for the primary disease. In addition there are readiographic methods valuable for the initiation of treatment, e. g. percutaneous antegrade pyelography and nephrostomy.

Topics: Adolescent; Glomerulonephritis; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Kidney Cortex Necrosis; Kidney Diseases; Male; Metabolic Diseases; Nephrocalcinosis; Oxalates; Phenacetin; Radiography

We measured urinary oxalate by the method of Hallson and Rose before and during long-term thiazide therapy in 49 patients with recurrent urolithiasis. Urinary oxalate excretion in normal men and women on their usual diets was 38.8 +/- 10.3 mg per day (mean +/- SD) and in patients with calcific renal calculi was 45.9 +/- 14.3 mg per day. Hydrochlorothiazide produced a significant decrease in urinary oxalate excretion in patients treated for more than 12 months (33 +/- 10.6 mg per day). We believe that the thiazide-induced reduction of urinary oxalate excretion is related to reduced intestinal calcium absorption which has been shown during chronic thiazide therapy and may not be evident until 12 or more months of thiazide administration.

Topics: Benzothiadiazines; Calcium; Diuretics; Female; Humans; Kidney Calculi; Male; Oxalates; Sodium Chloride Symporter Inhibitors; Time Factors

The formation of calcium oxalate crystals in rat kidneys was induced by intraperitoneal challenge with sodium oxalate. The structure of these crystals and the effect of their formation on the architecture of the tubular epithelium was studied by SEM. From the results we conclude that the crystals were formed intraluminally in the renal tubules. During the growth of the microliths they were closely adherent to the luminal surface of the tubular epithelial cells. Two types of the crystals were identified. Calcium oxalate monohydrate crystals consisted of plate-like crystallites and were more common. Dihydrate crystals on the other hand were tetragonal dipyramids and were less common. Elemental analysis of the crystal surface revealed them to be closely similar to the crystals present in calcium oxalate stones. The renal tubules were morphologically altered. Their epithelial cells underwent focal necrosis. There was a focal loss of the microvillous brush border of the proximal tubules. The epithelial cells formed large blebs which protruded into the tubular lumen. Sometimes the tubular lumen was completely occluded by the crystals. Crystals were often covered with cellular debris. It is suggested that the cellular debris derived from from necrotic cells become incorporated into the calculi. A similar process may be involved in the formation of mucoproteinaceus matrix of the human renal stones.

Topics: Animals; Electron Probe Microanalysis; Epithelium; Kidney Calculi; Kidney Cortex; Kidney Medulla; Kidney Tubules; Male; Microscopy, Electron, Scanning; Oxalates; Rats

Topics: Crystallography; Ethylene Glycols; Hydroxyapatites; Kidney Calculi; Kidney Tubules; Magnesium; Magnesium Deficiency; Microscopy, Electron, Scanning; Oxalates

Topics: Animals; Calcium; Calcium Oxalate; Calcium Phosphates; Cyclic AMP; Cystine; Cystinuria; Dehydration; Diet; Humans; Hydrogen-Ion Concentration; Hyperparathyroidism; Kidney Calculi; Male; Oxalates; Risk; Uric Acid; Urine

Weak electron paramagnetic resonance (EPR) signals from a number of calcium oxalate renal stones are attributed to an iron oxalate component. The g-value of the resonance is 2.0036 and its width is approximately 9 gauss. The EPR resonance from stones has the same characteristics as resonances from iron introduced into calcium oxalate and oxalic acid as an impurity. A sharp increase in EPR signal when calcium oxalate renal stones are exposed to intense light is attributable to the reduction of Fe3+ and the formation of the oxalate radical ion (C2O4)-.

Topics: Calcium Oxalate; Chemical Phenomena; Chemistry; Electron Spin Resonance Spectroscopy; Humans; Iron; Kidney Calculi; Oxalates

Topics: Calcium, Dietary; Cholestyramine Resin; Colon; Dietary Fats; Humans; Ileal Diseases; Ileitis; Intestinal Absorption; Kidney Calculi; Oxalates; Oxalic Acid; Solubility

Topics: Calcium; Crystallization; Humans; Kidney Calculi; Oxalates; Uric Acid

An 18-year-old female with primary oxalosis, seen first when she was in advanced renal failure, developed a severe necrotizing angiopathy which began after a rapid decrease in renal function requiring chronic dialysis. Because of the severe angiopathy the preliminary diagnosis of an acute autoimmune vasculitis had been made. The correct diagnosis was revealed by renal biopsy and a renal transplantation performed. Soon after severe oxalosis led to failure of the renal transplant and death. The patient had also had familial spherocytosis, inherited from her father, while the oxalosis had been inherited from her mother. It is suggested that early transplantation at the onset of renal failure, as long as the blood oxalate level is still tolerably low, may give better results than have so far been reported.

Topics: Adolescent; Female; Humans; Kidney Calculi; Kidney Failure, Chronic; Kidney Transplantation; Metabolism, Inborn Errors; Oxalates; Spherocytosis, Hereditary; Vascular Diseases

Topics: Child; Child, Preschool; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Humans; Infant; Kidney Calculi; Male; Metabolic Diseases; Nephrocalcinosis; Oxalates; Radiography

The biochemical findings in urine from 62 male and 20 female consecutive patients with renal stone disease were studied in relation to the size of concrements and the estimated rate of stone formation. There appeared to be good agreement between urine composition and stone history. Biochemical grouping of the patients resulted in different distributions in the different groups of stone-formers. The quotients calcium/magnesium (k1) and calcium X oxalate/magnesium X creatinine (k3) appeared to reflect the severity of stone disease and seemed to provide a rational approach to the evaluation of patients with urolithiasis.

Topics: Calcium; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Sex Factors; Uric Acid

Topics: Acidosis, Renal Tubular; Aged; Calcium; Calcium, Dietary; Cystinuria; Diet; Humans; Intestinal Diseases; Intestine, Small; Kidney Calculi; Male; Oxalates; Phosphorus; Uric Acid; Urinary Calculi

A formal protocol, controlled metabolic evaluation is essential to the most effective treatment of any patient with renal calculi, regardless of the crystalline composition of the stone. The design of the protocol and of the data sheets should be compatible with ease of diagnosis and selection of corrective therapeutic measures. These data also serve as a reference to monitor response to treatment. Treatment is highly individualized with the objective to reduce all potentially crystallizable ions to basal levels. If this is difficult to accomplish certain ratios of ions are brought to as near normal values as possible.

Topics: Adult; Calcium; Cystine; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Quaternary Ammonium Compounds; Uric Acid

A model system is described for the induction of renal calcium oxalate crystals with intraperitineal injections of sodium oxalate in rats. Early crystals are formed predominantly in cortical areas. Massive amounts of calcium are associated with this process, as demonstrated by potassium pyroantimonate staining. Actual crystal formation appears to be an involved process associated with calcium, oxalate, and cellular membranes. Although overt stone formation was not observed, we feel that the intimate involvement of membranes during crystal formation may be similar to that found in renal stones.

Topics: Animals; Calcium Oxalate; Crystallization; Kidney; Kidney Calculi; Male; Oxalates; Rats; Sodium; Time Factors

The early phases of calcium oxalate crystal formation in rat kidneys after intraperitoneal challenge with sodium oxalate were examined. From the results we conclude that the crystals are formed intraluminally in the proximal tubules of the renal cortex. The size, number, and distribution of calcium oxalate particles depend on the amount of sodium oxalate injected and the time interval after its injection. Tubular necrosis and dilation were evident after administration of higher doses of sodium oxalate. The papillary tip and corticomedullary junction were the preferential sites for crystal localization after longer periods of injections of higher doses of sodium oxalate.

Topics: Animals; Birefringence; Calcium Oxalate; Injections, Intraperitoneal; Kidney Calculi; Kidney Cortex; Kidney Tubules, Proximal; Male; Oxalates; Rats; Time Factors

Solubility measurements, seeded crystal growth kinetics, solution depletion adsorption studies, nucleation observations, zeta potential measurements, and measurements of in vivo intrarenal crystallization all failed to show that either oxipurinol or allopurinol riboside interacts with calcium, oxalate, or whewellite (CaC2O4.H2O) at concentrations expected in therapeutic situations. We conclude that at therapeutically expected concentrations, oxipurinol and allopurinol riboside do not affect crystallization of calcium oxalate.

Topics: Allopurinol; Animals; Calcium Oxalate; Crystallization; In Vitro Techniques; Kidney Calculi; Kinetics; Oxalates; Oxypurinol; Pyrimidines; Rats; Ribonucleosides

Topics: Humans; Ileum; Jejunum; Kidney Calculi; Obesity; Oxalates; Postoperative Complications

Topics: Adult; Creatinine; Female; Humans; Kidney Calculi; Oxalates; Pyridoxine

Topics: Child, Preschool; Diseases in Twins; Female; Humans; Kidney Calculi; Male; Oxalates; Pregnancy; Twins; Twins, Monozygotic

Topics: Calcium; Crystallization; Cyclic AMP; Female; Humans; Kidney Calculi; Male; Oxalates; Recurrence; Uric Acid

Topics: Adult; Ambulatory Care; Calcium; Calcium, Dietary; Cyclic AMP; Diagnosis, Differential; Fasting; Female; Hospitalization; Humans; Hypercalcemia; Kidney; Kidney Calculi; Male; Oxalates; Parathyroid Hormone; Phosphates; Uric Acid

Topics: Adult; Calcium; Cystine; Cystinuria; Humans; Hypercalcemia; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Uric Acid

Kinetics of growth and dissolution of calcium oxalate monohydrate were examined in the presence of small concentrations of methylene blue. The data presented show moderate retardation in growth and dissolution rates. It was also found that methylene blue decreased the decalcification rate of calcium oxalate renal calculi. The implications of these findings in the treatment of urolithiasis are discussed.

Topics: Calcium; Crystallization; Decalcification Technique; Humans; Kidney Calculi; Methylene Blue; Oxalates; Solubility

Topics: Calcium; Crystallography; Humans; Kidney Calculi; Microscopy, Polarization; Microtomy; Oxalates

Topics: Allopurinol; Humans; Kidney Calculi; Oxalates

A large number of trace elements has been found in calcium stones (whewellite, weddellite, and apatite) and in struvite. Significantly fewer elements, with lower abundances, are found in uric acid and cystine. With the exception of four trace elements (lead, silicon, strontium, and zine), the trace element assemblages are identical in the oxalates (whewellite and weddellite); struvite is also similar but with notable exceptions. In general, apatite contains approximately twice the level of trace element abundances as do the oxalates. This study is based on the distribution of 20 elements in 186 mimeralogically identified urinary calculi from three generalized areas of the United States (northeast, southeast, and midwest). In general, there is no statistical difference in the trace element assemblages of mineralogically identical stones from the three areas.

Topics: Aluminum; Apatites; Calcium; Calcium Oxalate; Cystine; Humans; Kidney Calculi; Magnesium; Oxalates; Phosphates; Quaternary Ammonium Compounds; Silicon; Trace Elements; United States; Uric Acid; Zinc

1. The possible roles of the diet and of intestinal absorption in the increased excretion of oxalate by patients with renal calcium stones have been studied. 2. Dietary surveys showed that the mean daily intake of oxalic acid by stone-formers was not significantly different from that of non-stone-formers. 3. The mean urinary excretion of oxalate, expressed as an oxalate/creatinine molar ratio, was significantly reduced by fasting, the change being more marked in the stone-formers than in the normal subjects. Moreover, fasting abolished the difference in mean oxalate/creatinine ratios between stone-formers and control subjects. 4. These results are compatible with the hypothesis that the small increases in urinary oxalate excretion which occur in some idiopathic calcium oxalate stone-formers are due to increased absorption of oxalate from the intestine, which may be due to a reduction in intraluminal calcium concentration.

Topics: Adult; Aged; Calcium, Dietary; Diet; Fasting; Humans; Intestinal Absorption; Kidney Calculi; Male; Middle Aged; Oxalates

The renal stones of 377 patients from the Brussels' area have been studied by chemical methods; 239 stones were submitted to qualitative analysis and the other 138 to a quantitative analysis. The results of the study demonstrate that, in Belgium as well as in other Western countries like the USA and Great Britain, calcium oxalate, calcium phosphate and magnesium ammonium phosphate are, in decreasing order of frequency, the major constitutents of renal calculi. The fact that calcium oxalate-containing stones are mainly found in men associated with sterile urine, and magnesium ammonium phosphate stones in women associated with urinary infection, is confirmed in the present series. The percentage of uric acid-containing stones is similar to that in the USA and Great Britain, but lower than that observed in several European countries including France, Spain, Germany, Czechoslovakia and Sweden. A small group of Mediterranean patients living in Belgium show no specific pattern, suggesting that the formation of calculi could be more dependent upon environmental than upon ethnic factors.

Topics: Ammonia; Belgium; Calcium; Calcium Phosphates; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Uric Acid

Topics: Administration, Oral; Adolescent; Adult; Child; DEAE-Cellulose; Drug Evaluation; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates

Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following the oral administration of 5 mmol of stable oxalate. When sodium oxalate alone was given without divalent cations to patients in the fasting state, the urinary oxalate increased promptly (within 2 hours). The increase was more prominent and sustained in those with ileal disease (ileal resection or jujunoileal bypass); thus, 35 per cent of the orally administered oxalate eventually appeared in the urine in the group with ileal disease, 8 per cent in the group with stones (renal and absorptive hypercalciurias) and 9 per cent in the control group. This hyperexcretion of oxalate could be largely, but not totally, ameliorated by the concurrent oral administration of divalent cations. Although urinary oxalate decreased significantly following the oral administration of calcium or magnesium, hyperoxaluria persisted in most patients. The results suggested that the hyperabsorption of oxalate in ileal disease cannot be accounted for solely by an increased absorbable oxalate pool associated with calcium-fatty acid complexation. Moreover, although urinary oxalate decreased, urinary calcium increased concurrently when either calcium or magnesium was given. Thus, there was no significant change or increase in the urinary state of saturation with respect to calcium oxalate.

Topics: Administration, Oral; Calcium; Cations, Divalent; Crystallization; Humans; Ileum; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Magnesium; Oxalates

There is a paucity of literature concerning the origin of urinary stone disease. This report uses information currently available to examine the likelihood of urinary stone disease starting from free or fixed crystalluric particles. We conclude that stone disease in the renal tubules and renal pelvis cannot begin on unattached (free) particles. However, in conditions associated with stone formation, initiation of bladder stone disease on free particles seems quite likely.

Topics: Humans; Kidney; Kidney Calculi; Kidney Pelvis; Kidney Tubules; Models, Biological; Oxalates; Urinary Bladder Calculi; Urinary Calculi

This paper examines the kinetics of calcium deposition in rat kidneys after an intraperitoneal sodium oxalate injection. From the results we conclude that only a limited portion of tubular surface is available for adsorption of calcium oxalate crystals, that adsorpption of calcium oxalate crystals onto tubular epithelium is a process of greater than first order with regard to the dose, and that the washout of retained particles from the tubules is a first-order process as related to time. Also, we conclude that in these animals, which were subjected to a large oxalate challenge, the deposition of calcium oxalate crystals is virtually all intratubular.

Topics: Animals; Calcium; Disease Models, Animal; Dose-Response Relationship, Drug; Kidney; Kidney Calculi; Male; Oxalates; Rats; Sodium

Topics: Humans; Kidney Calculi; Oxalates

Concentration and excretion in 24-hour urine, as well as serum concentrations of Na, K, Mg, Ca, Cl, P, uric acid and citrate were investigated in 209 calcium oxalate stone patients and 42 stone-free patients. Especially the concentration values of the urine components, except for uric acid and citrate, were found to be significantly lower for calcium oxalate stone patients. 21% of the stone patients showed hypercalciuria; hypercalciuria combined with hyperuricuria was found in only 7.1% of the cases and a solitary hyperuricuria in only 17%. As for kidney cortex, kidney papilla and muscle tissue in 10 calcium oxalate stone patients and 10 stone-free patients, the concentrations of Na, K, Ca, Mg as well as some trace elements were determined quantitatively by means of neutron activation analysis. Statistic analysis yielded a significantly lower sodium content of the kidney cortex within the stone-carrying group. Mean values of the calcium concentration in stone patients were lower for papilla and muscle tissue than in the control group. For magnesium no clear differences were found. The iron content in the papilla and muslce tissue of stone patients was significantly lower.

Topics: Calcium; Citrates; Humans; Kidney; Kidney Calculi; Magnesium; Muscles; Oxalates; Potassium; Sodium; Uric Acid

Topics: Adolescent; Adult; Age Factors; Aged; Allopurinol; Calcium; Child; Child, Preschool; Crystallization; Diet; Female; Humans; Infant; Infant, Newborn; Kidney Calculi; Male; Middle Aged; Oxalates; Purines; Syndrome; Uric Acid

The case of a seven and a half-year-old girl with hyperglycinuria, oxalate nephrolithiasis, and a normal plasma amino acid pattern is presented. Hyperglycinuria amounted to 400 mg of glycine in 24 h urine and the stone was composed of calcium oxalate dihydrate. The metabolic relationship between glycine and oxalate is discussed. It is possible that the association of nephrolithiasis and hyperglycinuria was coincidental, although the case of familial hyperglycinuria with nephrolithiasis reported by De Vries and collaborators and our case suggest the possibility of a relationship between the aforesaid compounds in vivo.

Topics: Child; Female; Glycine; Humans; Kidney Calculi; Oxalates; Renal Tubular Transport, Inborn Errors; X-Ray Diffraction

Studies have been done on patients with recurrent renal calculous disease, measuring in addition to the usual serum and urine constituents the inhibiting capacity of the urine and the activity products of calcium oxalate, octocalcium phosphate and brushite. Studies on the 24-hour urine calcium, phosphorus and uric acid and serum calcium indicate no essential differences between patients with calcium oxalate, mixed or uric acid stones and normal individuals. We were unable to demonstrate a difference in the inhibiting capacity of the urine between normal individuals and patients with calcium oxalate calculi, and levels of saturation of urine with calcium oxalate were identical in the calcium oxalate stone patients and normal individuals. The degree of saturation of urine with calcium phosphate is significantly greater in stone patients.

Topics: Calcification, Physiologic; Calcium; Calcium Phosphates; Cartilage; Humans; Kidney; Kidney Calculi; Methods; Oxalates; Recurrence

Urine oxalate was determined by the enzymatic method, quality criteria were established, and 24h oxalate excretion measured in healthy control subjects and in patients suffering from calcium urolithiasis. The technique is highly reliable and can be practiced in every conventional clinical laboratory. There is no increase in 24h urine oxalate in calcium urolithiasis when related to body weight or lean body mass.

Topics: Humans; Kidney Calculi; Methods; Oxalates

The clinical features of eight cases of primary hyperoxaluria have been summarized. The possibility of different phenotypes is discussed. A reduction, but no normalization, of the oxalate formation during pyridoxine therapy was found. A renal transplantation performed in one of the patients failed because of the formation of nephrocalcinosis.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Follow-Up Studies; Glycolates; Glyoxylates; Humans; Infant; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates; Pedigree; Uremia; Ureteral Calculi

Topics: Adult; Humans; Kidney Calculi; Male; Oxalates

Topics: Amyloidosis; Bile Acids and Salts; Celiac Disease; Cholelithiasis; Cholestyramine Resin; Colitis, Ulcerative; Crohn Disease; Gastrointestinal Diseases; Glycine; Hepatic Encephalopathy; Humans; Kidney Calculi; Kidney Diseases; Kidney Failure, Chronic; Malabsorption Syndromes; Oxalates; Proteinuria

Absorptive hypercalciuria was treated in 27 patients with cellulose phosphate. In all patients urinary calcium decreased and stone formation virtually ceased. The most striking side effect was an excessive hyperoxaluria, necessitating withdrawal of the drug in 8 patients. Succinate decreased the hyperoxaluria in 14 of 19 patients. All patients had mild hypercalciuria and hypermagnesiuria. This study was done to determine the therapeutic value and the side effects in the treatment of absorptive hypercalciuria with sodium cellulose phosphate and of hyperoxaluria with succinate.

Topics: Adult; Aged; Calcium; Cation Exchange Resins; Cellulose; Female; Humans; Intestinal Mucosa; Ion Exchange Resins; Kidney Calculi; Male; Middle Aged; Organophosphorus Compounds; Oxalates; Succinates

Topics: Adult; Benzothiadiazines; Calcium; Calcium, Dietary; Diuretics; Female; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Oxalates; Phosphates; Recurrence; Sex Factors; Sodium Chloride Symporter Inhibitors; Water

Topics: Adult; Calcium; Calcium Phosphates; Diphosphates; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence; Sex Factors

Oxalosis, a rare metabolic disorder, leads to excessive formation of oxalate and deposition of calcium oxalate crystals in the tissue. This leads to renal insufficiency with resulting secondary hyperparathyroidism and myelofibrosis. In a 27 year old female patient, extensive destruction of the maxilla, mandible and teeth was observed which has not yet been described and which led to the loss of all teeth.

Topics: Adult; Alveolar Process; Bone Resorption; Humans; Hyperparathyroidism; Jaw Diseases; Kidney Calculi; Kidney Failure, Chronic; Metabolism, Inborn Errors; Oxalates; Tooth Mobility; Tooth Resorption; Tooth Root

Calcium oxalate concretions grown in gelatin gel medium, and calcium oxalate renal stones were studied by polarized light and scanning electron microscopy. In both cases, the results obtained confirm that the surface crystals have random axial orientation and that the gross configuration seems to be determined by the fibrous organic matrix. In vitro concretions grown in the gelatin gel medium are more resistant to EDTA demineralization and to ultrasonic irradiation than calcium oxalate stones.

Topics: Calcium; Crystallization; Edetic Acid; Gels; Humans; In Vitro Techniques; Kidney Calculi; Microscopy, Electron, Scanning; Models, Biological; Oxalates; Ultrasonic Therapy

Topics: Humans; Ileum; Intestinal Diseases; Kidney Calculi; Oxalates

Intestinal bypass for obesity can be justified only if the risks of excess weight are higher than those of the surgery. Indications for this surgery need to be carefully defined and the patient and family should clearly understand the potential risks and benefits. Weight loss results from a decrease in food intake, altered taste preferences, and malabsorption. The benefits of this treatment are permanent weight loss, improved psychosocial function, and a reduction in medical morbidity. The potential risks consist of mortality, a variety of postoperative complications, liver failure, renal stones, and the consequences of bacterial overgrowth in the defunctionalized bowel. This operation trades the consequences of a short bowel for obesity and should only be undertaken where a skilled team of surgeons, internists, and psychiatrists are available and able to provide the necessary preoperative and postoperative managements.

Topics: Body Weight; Feeding Behavior; Female; Humans; Ileum; Intestinal Absorption; Intestines; Jejunum; Kidney Calculi; Liver Diseases; Male; Nutrition Disorders; Obesity; Oxalates; Postoperative Complications; Psychology, Social

Patients with ileal disease, ileal resection, and jejunoileal bypass are at increased risk of forming calcium oxalate renal calculi because of enhanced absorption of dietary oxalate. Intraluminal solubility of oxalate is an important determinant for hyperabsorption and may be regulated by intraluminal concentration of calcium and fatty acids. Malabsorbed bile salts and fatty acids may alter intestinal permeability, leading to increased passive diffusion of oxalate. Management includes a diet low in oxalate and fat content, dietary calcium of 750 mg/day, and cholestyramine.

Topics: Bile Acids and Salts; Calcium; Calcium, Dietary; Celiac Disease; Cholestyramine Resin; Dietary Fats; Fatty Acids; Humans; Ileum; Intestinal Diseases; Intestinal Mucosa; Jejunum; Kidney Calculi; Obesity; Oxalates

A review of the problems associated with extensive jejunoileal bypass for morbid obesity in a series of 175 carefully selected patients is presented. Five postoperative deaths occurred (3%). Nonfatal complications occurred in 21%, with wound infections (14 patients) being the most common. Good results marked by weight reduction to the range of ideal weight without significant electrolyte or metabolic aberrations was observed in 82% of the patients receiving the current dimensional modificatiom of end-to-end jejunoileal bypass (30 cm to 20cm). An additional 13% had fair results and only 5% had poor results. There were six deaths during follow-up: liver failure in four patients (secondary to alcohol abuse in two), myocardial infarction in one, and one from unknown causes. Bypass reversal was necessary for refractory liver failure in three patients (two from alcohol abuse), and for persistent diarrhea with secondary electrolyte depletion in two patients. One of these patients was complicated by severe emotional instability. This experience suggests that the majority of carefully selected patients will have a good response to jejunoileal bypass.

Topics: Adolescent; Adult; Anemia; Avitaminosis; Body Weight; Cholelithiasis; Diarrhea; Electrolytes; Fatty Liver; Female; Follow-Up Studies; Gout; Humans; Hypoproteinemia; Ileum; Jejunum; Kidney Calculi; Liver Diseases; Male; Middle Aged; Obesity; Oxalates; Postoperative Complications

Topics: Calcium; Crystallization; Humans; Kidney Calculi; Oxalates; Uric Acid

The effect of hydrochlorothiazide on the formation of renal stones was evaluated by quantitative assessment of the propensity of urine to undergo crystallization of calcium oxalate. In seven patients with calcium urolithiasis (three with absorptive hypercalciuria, one with renal hypercalciuria, and three with normocalciuric nephrolithiasis), the urinary activity product ratio and formation product ratio of calcium oxalate were measured both on and off therapy with hydrochlorothiazide (50 mg orally twice a day). The activity product ratio (state of saturation with respect to calcium oxalate) decreased in the majority of cases, primarily as a result of the fall in urinary calcium. The formation product ratio (limit of metastability) increased in all cases; the cause of the increase was not readily apparent. Both changes reduced the propensity of urine to undergo crystallization of calcium oxalate, and therefore may account for the clinical improvement reported during thiazide therapy in nephrolithiasis.

Topics: Adult; Aged; Calcium; Female; Humans; Hydrochlorothiazide; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates; Sulfates; Zinc

Initially, diarrhea is almost universal but becomes self-limited unless the patient persists in overeating. Weight loss averages 75 to 100 lb the first year, with a stable level generally achieved after 18 months. Among the serious potential complications are enteritis, kidney stones, gallstones, and hepatopathology. Some can be anticipated and kept at bay by prophylactic measures like high-protein intake.

Topics: Anti-Bacterial Agents; Arthritis; Body Temperature Regulation; Cholelithiasis; Dermatitis; Diarrhea; Dietary Proteins; Enteritis; Fatty Liver; Humans; Ileum; Intestinal Absorption; Kidney Calculi; Liver Diseases; Obesity; Oxalates; Postoperative Complications

Conventional and scanning electron microscopy of calcigerous renal calculi discloses typical concentric laminations, radial striations and microspherules. Random axial distribution of oxalate crystals and their coating by electron-dense matrix fibers with a definite parallel orientation and cross-linkages are evident. The biochemical relationship of uromucoid to matrix substance A is described. It is suggested that renal sialidase may convert the urinary uromucoid to matrix substance A, whose apatite-covered fibers may be responsible for epitaxial nucleation of some crystal systems. Our studies indicate that the intimate apatite-matrix relationship occurs in the human nephron, probably as an intracellular phenomenon. Subsequent extrusion of these mineralized complexes into the lumen of the nephron (intranephronic calculosis) may, in some instances, represent the initial microanatomic stage of renal calculogenesis.

Topics: Calcium Phosphates; Crystallization; Humans; Kidney Calculi; Mucoproteins; Oxalates

Topics: Calcium; Cystine; Humans; Kidney Calculi; Models, Chemical; Oxalates; Purines

The amino acid gamma-carboxyglutamic acid (Gla) is found in four blood-clotting proteins, in a bone protein, in kidney protein, and in the protein present in various ectopic calcifications. This paper reports the presence of Gla in the EDTA-soluble, nondialyzable proteins of calcium-containing renal calculi including calcium oxalate, hydroxyapatite, and mixed stores of apatite and struvite (MgNH4PO4). Calculi composed of pure struvite and those composed of only uric acid or cystine do not contain Gla. From calcium oxalate and hydroxyapatite stontes, a protein of about 17,000 daltons was obtained which contained about 40 residues of Gla per 1,000 amino acids. The amino acid composition of this protein had no apparent relationship to the Gla-containing bone protein or to the similarly-sized F1 fragment of prothrombin which contains about 64 residues of Gla per 1,000 amino acid residues. The Gla-rich protein in calcium-containing renal stones thus may be a different Gla-containing protein. These data as well as other studies demonstrating the presence of Gla in pathologically calcified tissues not normally containing Gla suggest that the Gla-containing proteins may be of considerable pathophysiological significance.

Topics: Adult; Amino Acids; Animals; Apatites; Calcium; Dogs; Glutamates; Humans; Kidney Calculi; Molecular Weight; Oxalates; Phosphates; Protein Binding; Proteins; Tricarboxylic Acids

Topics: Cholelithiasis; Crohn Disease; Humans; Ileum; Kidney Calculi; Male; Middle Aged; Oxalates; Postoperative Complications

Topics: Calcinosis; Humans; Kidney Calculi; Metabolic Diseases; Metabolism, Inborn Errors; Oxalates

Topics: Age Factors; Calcium; Child; Child, Preschool; Diet; Humans; India; Infant; Infant, Newborn; Kidney Calculi; Oxalates; Sex Factors; Socioeconomic Factors; Urinary Bladder Calculi

Topics: Crystallography; Electrons; Female; Humans; Kidney Calculi; Male; Microscopy, Electron; Molecular Conformation; Oxalates; Spectrum Analysis

A patient working as a stove-fitter suffers from calciumoxalate urolithiasis. The exploration of his typical occupation and the special investigation of lithogenic factors in urine and serum points to deterioration of oxalate urolithiasis.

Topics: Adult; Beverages; Environmental Exposure; Humans; Kidney Calculi; Male; Occupational Diseases; Occupations; Oxalates

Topics: Acrylates; Calcium; Cellulase; Drug Combinations; Humans; Kidney Calculi; Oxalates; Phosphates

Protective (inhibitory) effects of human urinary macromolecules on the crystallization of calcium oxalate were found when these urinary macromolecules were added to water or to salt solutions, which mimic human urine with respect to the concentrations of the most abundant small molecular weight species. The aspects of calcium oxalate crystallization affected by urinary macromolecules were: (i) an inhibition of nucleation (increased metastable limit), (ii) an inhibition of the crystallization rate, (iii) a decrease in the supersaturation level, and (iv) a decrease in adhesion of crystals to container surfaces.

Topics: Calcium; Crystallization; Humans; In Vitro Techniques; Kidney Calculi; Macromolecular Substances; Oxalates; Sodium Chloride; Urine; Water

By chronic intoxication with ethylene glycol or acute intoxication by Na-glyoxalate in the animal experiment a Ca-oxalatenephrolithiasis could be produced. At this model the influence of magnesium, pyridoxine and phosphate was studied. The combination therapy of magnesium and vitamin B6 can completely prevent the formation of Ca-oxalate-microliths in the kidney. The production of a preparation with 200 mg MgO and 10 mg pyridoxine per tablet for the metaphylaxis of oxalate calculi is recommended.

Topics: Animals; Calcium; Chelating Agents; Female; Kidney Calculi; Magnesium; Oxalates; Oxidative Phosphorylation; Pyridoxine; Rabbits

Two hundred two recurrent calcium oxalate stone-forming patients with idiopathic hypercalciuria or hyperuricosuria, or both, were treated for an average of 2.91 years (1 to 7 years) with thiazide or allopurinol, or both. The frequency of new stone formation was drastically reduced. During the treatment period of 625 patient years, 220.0 new stones should have occurred, whereas 22 were actually formed (chi-square=178, P less than 0.001). Thirty-four patients without discernible metabolic disturbances and treated only with increased fluid intake and dietary advice formed 29 new stones compared to a predicted 33.2 stones (87.3%). Thirty similar patients treated with thiazide and allopurinol formed six stones compared to a predicted 31.8, P less than 0.001. Chronic reversal of idiopathic hypercalciuria and hyperuricosuria with thiazide and allopurinol is an effective way to prevent recurrent calcium oxalate stones. Conservative measures are only of marginal effectiveness in treating metabolically normal stone forming patients; however, thiazide and allopurinol appear to decrease new stone formation.

Topics: Allopurinol; Calcium; Cystoscopy; Female; Hospitalization; Humans; Kidney Calculi; Male; Metabolic Diseases; Oxalates; Recurrence; Trichlormethiazide; Uric Acid

A patient who underwent jejunoileal bypass for morbid obesity developed servere renal failure associated with hyperoxaluria and renal oxalosis. Renal function improved and oxalate excretion decreased following hemodialysis and restoration of gastrointestinal continuity.

Topics: Acute Kidney Injury; Humans; Ileum; Jejunum; Kidney Calculi; Kidney Glomerulus; Male; Microscopy, Electron; Middle Aged; Obesity; Oxalates; Postoperative Complications; Renal Dialysis

Topics: Adult; Humans; Ileum; Kidney Calculi; Male; Oxalates

Several serum and urinary constitutents were evaluated in 13 calcium oxalate kidney stone formers in whom according to urinary vitamin B6 excretion sufficient vitamin B6 intake before the study was suggested. The influence of 28-day Pyridoxine (Spofa) supplementation (20 mg three times daily) on these biochemical parameters was searched. Pyridoxine supplementation was followed by a significant increment in the mean values of serum uric acid; the remaining serum constitutents did not change. Urinary calcium, phosphare, magnesium, sodium, potassium, and uric acid slightly increased, urinary oxalate excretion slightly fell; there was a high variability in the changes between the individuals. No changes in the mean values of clearance of endogenous creatinine, percentage of tubular reabsorption of phosphate and urinary zinc excretion were found. It is suggested that long-term studies are necessary to search the factors influencing successful stone prevention or stone recurrency in pyridoxine-treatment patients.

Topics: Adolescent; Adult; Calcium; Creatinine; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Potassium; Pyridoxine; Sodium; Uric Acid

Topics: Calcium Phosphates; Chemical Precipitation; Crystallization; Hydrogen-Ion Concentration; Hydroxyapatites; Kidney Calculi; Oxalates; Uric Acid

A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.

Topics: Demyelinating Diseases; Humans; Kidney Calculi; Kidney Failure, Chronic; Male; Median Nerve; Metabolic Diseases; Middle Aged; Nephrectomy; Nerve Fibers, Myelinated; Oxalates; Peripheral Nerves; Peripheral Nervous System Diseases; Radial Nerve; Renal Dialysis; Schwann Cells; Sciatic Nerve

Histological and biochemical studies were carried out in a total of 300 patients who had died in the recovery room, and in rabbits, to investigate the frequency of deposits of calcium oxalte crystals in the kidneys, the influence of infusion therapy and the pathological significance of such deposits on the kidney tissue and on renal function. - Quite independent of any infusions, however, deposits of calcium oxalate crystals were found in the presence of kidney-specific diseases, in particular uraemia and anuric conditions. Xylitol infusions of 0.4 g/kg body weight or, in individual cases, of not more than 500 g total in 7 days, had no infllence on the appearance of calcium oxalate deposits. The blockage of the tubular system by the calcium oxalate deposits leads to a temporary reversible increase in serum urea and serum creatinine. With time, and uninfluenced by infusions, the deposits disappear out of the kidney again without having caused any organic renal damage. In the presence of a temporary excess of serum oxalate, the kidneys temporarily act like a cloaca.

Topics: Animals; Anuria; Autopsy; Calcium; Humans; Injections, Subcutaneous; Kidney; Kidney Calculi; Kidney Diseases; Oxalates; Parenteral Nutrition; Rabbits; Uremia; Xylitol

In a total of 45 deceased persons, 33 cases showed no intrarenal crystal deposition and in 12 cases morphological investigation revealed intrarenal crystal deposition of varying intensity. All patients with crystal deposition had received considerable quantities of xylitol infusions within a period of 10 days. The possible connection between infusion of xylitol-containing solutions and intrarenal crystal deposition is discussed in detail.

Topics: Adolescent; Autopsy; Humans; Kidney Calculi; Kidney Diseases; Kidney Tubules; Nephrosis; Oxalates; Parenteral Nutrition; Xylitol

Topics: Amino Acids; Calculi; Glycine; Humans; Kidney Calculi; Oxalates; Parenteral Nutrition; Sorbitol; Urinary Calculi; Wounds and Injuries; Xylitol

Topics: Calcium; Carbon Radioisotopes; Crystallization; Dialysis; Humans; Kidney Calculi; Mucoproteins; Oxalates

Topics: Adolescent; Adult; Anemia, Hypochromic; Avitaminosis; Cholelithiasis; Diarrhea; Female; Follow-Up Studies; Gout; Humans; Ileum; Jejunum; Kidney Calculi; Liver Diseases; Male; Middle Aged; Obesity; Oxalates; Postoperative Complications

After World War II the incidence of urolithiasis increased consistently among the general population in this country. Nearly 25% of all examined renal calculi contain uric acid, sodium acid urate or ammonium acid urate as constituents. There are two peaks in lifespan of occurring urate stones: in the adolescence and in the age between 40 and 60 years. The following conditions are due to the formation of uric acid-containing stones: 1. Gout and primary hyperuricemia; 2. secondary hyperuricemia; 3. idiopathic cases with normal renal excretion of uric acid and normouricemia, but with a higher degree of acidity of the urine than normal considering the total renal excretion of acid products; 4. iatrogenic hyperuricemia during insufficient uricosuric therapy. Up to more than 30% of all the patients with recurrent formation of oxalate stones show a clear association with hyperuricemia, hyperuricosuria and increased renal excretion of calcium. In the presence of sodium urate a considerable promotion of precipitation of crystals consisting of calcium oxalate from a meta-stable solution may occur (so-called epitaxy). Frequently the existence of uric acid stones is without any symptoms. Modern views with regard to prophylactic procedures, diet, general and specific medical management including surgical intervention are presented.

Topics: Calcium; Gout; Humans; Kidney Calculi; Oxalates; Uric Acid

Investigation of multiple serum and urinary factors in 44 patients with calcium urinary stone disease confirmed a number of defects that have been described previously: elevation of mean serum calcium and uric acid above normal, and depression of mean serum magnesium. Urinary excretion of calcium and uric acid was increased and was increased and was probably related to food ingestion. Urinary magnesium also increased after eating but less than calcium, with the result that for most patients the magnesium to calcium x 100 ratio approached levels observed in stone formation. Urinary oxalate excretion was constant during the entire observation period and apparently was not affected by ingestion of a defined diet. Nine additional patients had persistent hypercalcemia owing to hyperparathyroidism (5 confirmed, 1 suspected), malignancy (2) and drug ingestion (1). Metabolic evaluation of patients with calcium urinary calculi continues to contribute to decisions regarding their best therapeutic regimen.

Topics: Calcium; Diet; Female; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Magnesium; Male; Oxalates; Uric Acid

The authors report a case of regional enteritis complicated by nephrocalcinosis and nephrolithiasis. Enteric hyperoxaluria is documented and the pathophysiology is discussed.

Topics: Adult; Crohn Disease; Humans; Kidney Calculi; Middle Aged; Nephrocalcinosis; Oxalates; Radiography; Recurrence

Utilizing a low pyridoxine, ethylene glycol-fed rat model, various modes of anticalculus therapy were compared. Prophylactic papillary and parenchymal oxalate stone therapy is most effective with magnesium oxide. Hydrochlorothiazide is next in order as the therapy of choice in this group. A high calcium diet seems to negate the effect of magnesium oxide. Methylene blue, magnesium oxide, and even sodium phosphate, are not as effective as hydrochlorothiazide in the combined prevention and treatment of preformed parencymal calcium oxalate stones. No agent seems to have a profound effect on preformed apical papillary calculi.

Topics: Animals; Disease Models, Animal; Hydrochlorothiazide; Kidney Calculi; Magnesium Oxide; Male; Methylene Blue; Oxalates; Phosphates; Rats

Inadvertent use of tetracycline hydrochloride while producing calcium oxalate stones in the rat resulted in a reduction of papillary concretions by one-half. Parenchymal calcifications in the continuing long term, preformed stone group were reduced to levels comparable to that of other useful agents. In vitro studies corroborated these findings at physiologic urinary pH ranges. The rationale and comparisons to other anticalculus drugs are discussed.

Topics: Animals; Calcium; In Vitro Techniques; Kidney Calculi; Oxalates; Rats; Tetracycline

Topics: Female; Humans; Kidney Calculi; Male; Oxalates

In a child with renal failure and oliguria due to hyperoxaluria myelophthisis developed as a result of extensive bone-marrow replacement with calcium oxalate crystals and an accompanying fibrous proliferations. The histopathology associated with this metabolic disorder was demonstrated in posterior iliac crest bone-marrow trephine biopsies, renal biopsies, and nephrectomy specimens. Crystals were demonstrated in biopsy specimens of transplanted kidneys within six weeks following renal transplantation.

Topics: Anemia, Myelophthisic; Bone Marrow; Child, Preschool; Female; Humans; Kidney; Kidney Calculi; Metabolism, Inborn Errors; Oxalates

In a group of 57 children with urolithiasis hypomagnesaemia was found in 15 cases (26.3%). All children but one with abnormally low serum magnesium levels had recurrent or bilateral nephrolithiasis or nephrocalcinosis. Prevalence of hyperoxaluria and hypercalciuria, marked severity of the clinical features, abnormality of Ca metabolism and its responsiveness to MgO treatment were demonstrable in Mg deficiency.

Topics: Adolescent; Calcium; Child; Child, Preschool; Czechoslovakia; Humans; Infant; Kidney Calculi; Magnesium Deficiency; Oxalates; Recurrence

Kidney tissue enzyme patterns from patients with calcium oxalate stone disease were compared to enzyme patterns from healthy and inflamed human kidneys. In the case of oxalate stone disease there was a significantly decreased activity of the glycolytic enzyme aldolase, resulting in a cumulation of oxaloacetate and of oxalic acid. This decrease of the aldolase activity does not completely reveal the cause of calcium oxalate stones but provides a new aspect to the disease.

Topics: Calcium; Carbohydrate Metabolism, Inborn Errors; Fructose-Bisphosphate Aldolase; Glyoxylates; Humans; Kidney; Kidney Calculi; Nephritis; Oxalates

24-hour urinary outputs of oxalate, calcium, and magnesium have been determined in a total of 62 children aged 3 months to 17 years who fell into the following groups: (i) 16 normal controls, (ii) 3 with primary hyperoxaluria, (iii) 9 with small and/or large intestinal resections, (iv) 9 with untreated coeliac disease, (v) 5 with pancreatic dysfunction, and (vi) a miscellaneous group of 20 children with a variety of intestinal disorders. Taken as a whole, 58% of patients with intestinal disorders had hyperoxaluria, and of these 7% had urinary outputs of oxalate which fell within the range seen in primary hyperoxaluria. The proportion of children with hyperoxaluria in the different diagnostic groups was as follows: intestinal resections (78%), coeliac disease (67%), pancreatic dysfunction (80%), and miscellaneous (45%). 35% of the patients with hyperoxaluria had hypercalciuria, whereas magnesium excretion was normal in all subjects studied. In 2 patients treatment of the underlying condition was accompanied by a return of oxalate excretion to normal. These results indicate that hyperoxaluria and hypercalciuria are common in children with a variety of intestinal disorders, and that such children may be at risk of developing renal calculi without early diagnosis and treatment.

Topics: Adolescent; Calcium; Celiac Disease; Child; Child, Preschool; Colon; Glutens; Humans; Infant; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Liver Diseases; Magnesium; Oxalates; Pancreatic Diseases

Thermogravimetric (TG) analysis has been used as a routine technique for renal tract stone analysis. The results obtained in a consecutive series of 502 renal stones are described and evaluated. The technique is easy, rapid and gives quantitative information about stone composition. Results were compared with quantitative data obtained by standard chemical methods. Correlation coefficients for oxalate and urate were o-947 and 0-97 respectively. The comparison also showed that 63% of the stones could have been correctly analysed by TG analysis alone; in an additional 31%, TG analysis provided helpful information. TG analysis permits the identification of the proportions of mono- and dihydrate of oxalate present in calcium oxalate. It is confirmed that the centres of calcium oxalate calculi are richer in dihydrate than the exterior surfaces.

Topics: Calcium Phosphates; Chemistry Techniques, Analytical; Humans; Kidney Calculi; Oxalates; Thermogravimetry

Topics: Adult; Calcium; Diet; Humans; Kidney Calculi; Male; Oxalates; Purines; Uric Acid

Topics: Arrhythmias, Cardiac; Barbiturates; Butyrylcholinesterase; Drug Synergism; Drug Tolerance; Dysautonomia, Familial; Genetic Diseases, Inborn; Humans; Hyperbilirubinemia, Hereditary; Jaundice; Kidney Calculi; Malignant Hyperthermia; Metabolism, Inborn Errors; Narcotics; Nephrocalcinosis; Osteogenesis Imperfecta; Oxalates; Paralyses, Familial Periodic; Pharmacogenetics; Porphyrias; Succinylcholine

Topics: Humans; Kidney Calculi; Minerals; Oxalates; Phosphoric Acids; Recurrence; Ureteral Calculi; Uric Acid

Topics: Calcium; Humans; Intestinal Absorption; Kidney Calculi; Oxalates; Parathyroid Diseases

Topics: Animals; Kidney Calculi; Kidney Tubules; Male; Mice; Microscopy, Electron, Scanning; Oxalates

An experimental electron-microscopic study of the kidneys was carried out in experimental oxamide nephrolithiasis in rabbits and hypervitaminosis D in rats. The most pronounced changes were revealed in the proximal and the distal convoluted tubules. It is suggested that cytosomes and lysosome-like bodies possibly participated in stone formation and nephrocalcinosis. It is supposed that they played an important role in the morphogenesis of nephrolithiasis man.

Topics: Animals; Ergocalciferols; Kidney; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Rabbits; Rats

Topics: Calcium; Crystallization; Cystine; Cystinuria; Humans; Kidney Calculi; Oxalates; Uric Acid

Topics: Calcium; Diuretics; Humans; Kidney Calculi; Oxalates; Phosphates; Phytic Acid

Jejunoileal bypass for obesity has been shown to be associated with increased hepatic triglycerides during the period of brisk weight loss. The current report describes certain metabolic changes observed in 29 patients 21 months after bypass. Significant decreases in serum cholesterol, serum triglycerides, blood sugar after a glucose load, and fasting plasma insulin levels were noted. Increased oxalate excretion and occasional episodes of hypomagnesemia occurred. Repeated clinical and laboratory observations by a medical-surgical team offer the best opportunity to evaluate this procedure.

Topics: Adolescent; Adult; Alkaline Phosphatase; Aspartate Aminotransferases; Body Weight; Evaluation Studies as Topic; Feces; Female; Glucose Tolerance Test; Humans; Ileum; Insulin; Jejunum; Kidney Calculi; Lipid Metabolism; Magnesium; Male; Middle Aged; Obesity; Oxalates; Postoperative Complications

Organic matrices from kidney stones of several mineral compositions (calcium oxalate, uric acid, and apatite-struvite) were isolated and found to contain an abundance of acidic amino acids. The calcium oxalate stones contained 50% aspartic and glutamic acid residues while the uric acid stones contained over 65%. The apatite-struvite stones had only 30% of these two amino acid residues and also contained 20% glycine residues. Since the specific amino acid composition differed for stones of different mineral content, it was felt that the organic matrix might play the role of a nucleating agent.

Topics: Amino Acids; Apatites; Calcium; Calcium Phosphates; Humans; Kidney Calculi; Magnesium; Molecular Weight; Oxalates; Phosphates; Proteins; Quaternary Ammonium Compounds; Uric Acid

The physicochemical factors involved in the formation of calcium-containing renal stones have been elucidated previously and some of the techniques for their quantitation are currently available. Accordingly, urinary activity product ratio (state of saturation), formation product ratio (limit of metastability), and crystal growth of brushite and calcium oxalate in 24-hr urine samples were compared between a control group without stones and stone-forming groups composed of patients with absorptive hypercalciuria, normocalciuric nephrolithiasis, and primary hyperparathyroidism. The activity product ratios of brushite and calcium oxalate were significantly elevated in stone-forming groups, largely because of the high renal excretion of calcium. The formation product ratios were reduced in most stone-forming groups, and the crystal growth was increased in the group with primary hyperparathyroidism. Thus, the physicochemical environment of urine in stone-forming groups was favorable to the nucleation of the nidi of brushite and calcium oxalate; in primary hyperparathyroidism, it may be conducive to the subsequent growth of nidi as well.

Topics: Adult; Calcium Metabolism Disorders; Calcium Phosphates; Crystallization; Female; Humans; Hyperparathyroidism; Kidney Calculi; Male; Oxalates

Any patient presenting with renal colic requires the taking of a detailed history-- with inquiries about diet and drugs, an examination of the urine, intravenous pyelography and measurement of the calcium concentration in serum and urine. Any stone passed should be analysed. Recurrent stone formation warrants more comprehensive metabolic investigation. The cause of renal calculi in most patients is still not known. When a cause is found, specific treatment can prevent or control stone formation. For the majority in whom no abnormality is detected, various methods of reducing stone formation have been tried but results are disappointing. The most important points in management are the early detection and effective treatment of urinary tract infection or obstruction and the maintenance of a high fluid intake.

Topics: Bacteriuria; Calcium; Child; Cystinuria; Humans; Kidney Calculi; Male; Oxalates; Uric Acid

Knowledge of the crystalline structure of the calculus provides the basis of the therapeutic plan. Laboratory evaluation depends heavily upon routine urinalysis. Assessment of renal function, serum calcium, phosphorus, uric acid and, in some cases electrolytes is usually indicated, as is urography. General principles of management include maintenance of an ample urine volume, eradication of infection and correction of any obstructing lesions or metabolic abnormalities. Specific antistone regimens are indicated for patients with recurrent urolithiasis.

Topics: Anti-Bacterial Agents; Calcium; Cystinuria; Diarrhea; Female; Humans; Hydrochlorothiazide; Intestinal Diseases; Kidney Calculi; Male; Oxalates; Phosphates; Proteus Infections; Uric Acid; Urinary Calculi

Topics: Acidosis; Ascorbic Acid; Blood; Cholesterol; Gastrointestinal Diseases; Glycosuria; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Kidney Calculi; Oxalates; Prothrombin; Vitamin B 12

The radiological changes in a patient with endogenous oxalosis are correlated with their pathological and anatomical counterparts. These involve particulary the kidneys (nephrolithiasis, calcium oxalate nephrosis with scarring), the skeleton (combination of renal osteodystrophy, secondary hyperparathyroidism and oxalate deposition), and soft tissues (generalised oxalate deposition). The pathological aspects described in the literature are mentioned and possible forms of treatment are stressed.

Topics: Adult; Bone and Bones; Humans; Hyperparathyroidism; Kidney Calculi; Kidney Diseases; Metabolic Diseases; Nephrocalcinosis; Nephrosclerosis; Nephrosis; Oxalates; Radiography

Topics: Adult; Age Factors; Blood Chemical Analysis; Calcium; Child; Citrates; Cystinuria; Diet Therapy; Female; Humans; Hydrochlorothiazide; Hydrogen-Ion Concentration; Kidney Calculi; Malabsorption Syndromes; Male; Medical History Taking; Oxalates; Phosphorus; Racial Groups; Recurrence; Sex Factors; Uric Acid; Urinary Tract Infections; Urine; Urography

Reliable techniques for the calculation of activity product (state of saturation), formation product (limit of metastability) and crystal growth of calcium oxalate were devised. The activity product at saturation was 2.53 times 10 minus 9 M2, and was independent of duration of incubation, solid-to-solution ratio, pH, calcium concentration or ionic strength. These tehcniques were utilized to assess the effect of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) on crystallization of calcium oxalate in an aqueous salt solution in vitro. EHDP increased the formation product of calcium oxalate, indicating an inhibition of nucleation of calcium oxalate. Further, it inhibited the crystal growth of calcium oxalate.

Topics: Calcium; Crystallization; Etidronic Acid; Hydrogen-Ion Concentration; In Vitro Techniques; Kidney Calculi; Organophosphonates; Organophosphorus Compounds; Oxalates; Solubility; Spectrophotometry, Atomic

The findings of serum diagnosis (urea nitrogen, creatinine, uric acid, calcium, phosphorus) in 247 patients with oxalate stone were divided according to sex, and the excretion of uric acid, calcium and phosphorus was estimated. Compared with the control group, the levels of serum uric acid and serum calcium were statistically significantly raised, the mean level not exceeding the normal range. The serum uric acid level was 25% above the normal range in men and 20% above in women, and in the upper range of normal in one third of each, men and women. The excretion of uric acid in women exceeds the normal level in 32% of cases and in 40% of the men, sometimes considerably. The connection between pathological uric acid levels in the serum and urine and the development of oxalate stone, as well as the therapeutic consequences are discussed.

Topics: Adult; Aged; Allopurinol; Calcium; Creatinine; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphorus; Uric Acid; Uricosuric Agents

The diangosis, clinical manifestations and management of 11 children with nephrocalcinosis encountered in a 20-year period are presented. Renal tubular acidosis, primary hyperoxaluria, primary hyperparathyroidism, exogenous hyperadrenocorticism and idiopathic hypercalcemia of infancy were the principal causes of nephrocalcinosis in this series. In the presence of normal or near-normal renal function, a 55 per cent or better cure rate can be expected. Children with significantly diminished renal function have a poor prognosis and should be considered for renal transplantation.

Topics: Acidosis, Renal Tubular; Adolescent; Child; Child, Preschool; Cushing Syndrome; Female; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Kidney Transplantation; Male; Nephrocalcinosis; Oxalates; Prognosis; Transplantation, Homologous; Ureteral Calculi

The present status of regular dialysis and renal transplantation in patients with end-stage renal disease secondary to primary hyperoxaluria is reported. Clinical studies include one personal case with an 18-month period of follow-up and data concerning thirteen patients treated in 10 centres in Europe which have been collected through a cooperative survey carried out with the assistance of Registry of the EDTA. On January 1 st, 1974, mean survival of patients with oxalosis treated by RDT was 30.4 months (range 6 to 102 months). Five cadaveric renal transplants have been performed in four patients; two patients are surviving with grafts functioning for 18 and 45 months. Dialysis and/or transplantation should be performed in patients with oxalosis early enough to prevent ischaemic, cardiac and neuromusclar complications which occur at the end-stage of the disease. Evidence for blood coagulation disorders, particularly chronic consumption coagulopathy, should be investigated for with adequate laboratory methods and long-term heparin therapy instituted if necessary. No convincing reports concerning the efficiency of the various drugs which have been tried out to reduce the biosynthesis of oxalic acid in patients with oxalosis have been issued to this date.

Topics: Acute Kidney Injury; Adolescent; Adult; Arrhythmias, Cardiac; Child; Child, Preschool; Disseminated Intravascular Coagulation; Extremities; Female; Humans; Ischemia; Kidney Calculi; Kidney Transplantation; Male; Metabolic Diseases; Middle Aged; Neuromuscular Diseases; Oxalates; Renal Dialysis

Topics: Humans; Kidney Calculi; Oxalates

Obstruction is rarely accepted as the sole cause of calculi. We have reviewed 106 cases of nephrolithiasis for which surgery was performed at the St. Luke's Hospital Center during the past ten years. In 17 of these cases, obstruction of the ureteropelvic junction was demonstrated, an incidence of 16 per cent. We propose the theory that too frequently the responsible ureteropelvic junction obstruction goes undetected when a "routine" pyelolithotomy or nephrolithotomy is performed.

Topics: Adolescent; Adult; Aged; Calcium; Child; Female; Humans; Kidney; Kidney Calculi; Kidney Diseases; Kidney Pelvis; Male; Middle Aged; Oxalates; Ureteral Obstruction

The management of 78 children with upper urinary calculi is described. Boys outnumbered girls by a ratio of 2 to 1. Two-thirds of the patients had identifiable metabolic causes, while the remaining third had infected renal lithiasis. In this latter group, all patients had had multiple urologic procedures, urinary infection, and stasis with diversionary and indwelling drainage devices. Contrary to earlier views, idiopathic renal lithiasis with or without hypercalciuria was the most common metabolic form of nephrolithiasis in children. Sixty-seven patients (86 per cent) were followed for an average of 7 1/2 years. With appropriate therapy, stone disease became inactive in 70 per cent of the children. The remaining 30 per cent continued with active disease--5 died of renal failure and 1 has received a renal allograft. Stone formation may be regarded as a solitary complication or one of several manifestations of a large number of underlying disorders. Along with a thorough search for etiologic factors there must be an equally aggressive therapeutic effort. Because the disease is ofter sporadic, careful long-term followup of the patients with active as well as those with inactive stone disease is mandatory.

Topics: Acidosis, Renal Tubular; Adolescent; Adrenocortical Hyperfunction; Age Factors; Calcium; Child; Child, Preschool; Cystinuria; Female; Humans; Hypercalcemia; Hyperparathyroidism; Infant; Infant, Newborn; Kidney Calculi; Magnesium; Male; Metabolic Diseases; Oxalates; Uric Acid; Urinary Tract Infections; Urography

Topics: Cecum; Female; Glycolates; Humans; Ileostomy; Ileum; Intestinal Absorption; Jejunum; Kidney Calculi; Male; Obesity; Oxalates; Postoperative Complications

The mechanism of renal stone formation is not fully understood. This report describes an investigation into the effect of urine on the precipitation of calcium oxalate from dilute solution. Over 33 min a 5 per cent solution of urine caused considerable inhibition of precipitation. The degree of this inhibition was related to the concentration of the original urine. An "artificial urine" composed of 12 solutes present in normal urine had some inhibitory effect, but less than that of equiosmolar true urines. Inhibition was also related to the percentage of urine present. This inhibitory effect may be important in the prevention of renal stone formation in normal people by delaying crystallization until urine reaches the lower urinary tract.

Topics: Adolescent; Adult; Calcium; Chemical Precipitation; Crystallization; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Urine; Water

Topics: Carbon Radioisotopes; Gastrointestinal Diseases; Glycine; Glyoxylates; Humans; Intestinal Absorption; Intestine, Small; Kidney Calculi; Liver; Metabolic Diseases; Oxalates; Taurine

Out of a group of 979 patients with urinary calculi, 175 had passed their stone(s). Comparison of data for stones which had been passed with data for the whole group shows many significant differences. Calculi composed entirely of calcium oxalate are more likely to be expelled than any other composition variety. The chance of this happening is 1 in 3 and it is even higher when the person is under 50 years of age. The probability of calculi composed of calcium oxalate+calcium phosphate being expelled is 1 in 5 and this also increases for younger patients. Infection stones consisting of calcium phosphate+struvite have only 1 in 19 chance of being passed. Many of the stones passed (130) are under 0.10 g in weight. However, there is a similar relationshp between composition and weight among both the stones that were passed and the whole group. In both groups, pure oxalate stones are the lightest, infection stones are the heaviest and stones composed of calcium phosphate and calcium phosphate+calcium oxalate are of intermediate weight.

Topics: Adolescent; Adult; Age Factors; Aged; Calcium Phosphates; Child; Child, Preschool; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Sex Factors; Ureteral Calculi; Uric Acid; Urinary Calculi

Quantitative thermal analysis was carried out of 2300 calculi collected in Hungary. These included diverse mono-, di- and trimineral stones, spontaneously excreted and surgically removed whewellite and weddellite calculi. There percentage distribution among male, female and children patients, the regularities in the composition of mixed calculi and the incidence of falsifications are discussed in detail.

Topics: Adult; Age Factors; Calcium; Chemical Phenomena; Chemistry; Child; Female; Humans; Hungary; Kidney Calculi; Male; Oxalates; Sex Factors

Topics: Acidosis, Renal Tubular; Acute Disease; Analgesics; Calcium; Chronic Disease; Cystinuria; Female; Humans; Hyperparathyroidism; Infrared Rays; Kidney Calculi; Male; Oxalates; Radiography; Spectrum Analysis; Ureteral Calculi; Urinary Calculi; Urinary Tract Infections; X-Ray Diffraction

Topics: Adolescent; Adult; Alcohol Oxidoreductases; Biopsy; Bone and Bones; Carboxy-Lyases; Female; Glyceric Acids; Glycolates; Glyoxylates; Humans; Ketoglutaric Acids; Kidney; Kidney Calculi; Kidney Failure, Chronic; Kidney Tubules; Male; Metabolic Diseases; Methods; Microscopy, Polarization; Nephritis, Interstitial; Oxalates; Renal Artery Obstruction

Methylene blue in a dose of 65 mg. three times a day has been reported to be useful in the management of chronic renal calculous disease. Sixty-eight patients with renal calculi, in whom there was no biochemical abnormality, were started on this drug five or more years ago. Forty-six per cent of formers of calcium oxalate stone have passed no further stones, and 20 per cent have been improved. Initial studies had reported success in the management of infected stones. However, only 27 per cent obtained any benefit in this study. Methylene blue is useful in the management of patients who form multiple small calculi that contain calcium oxalate dihydrate and may be useful in the prevention of new stone formation.

Topics: Calcium; Humans; Kidney Calculi; Methylene Blue; Oxalates

Randall described a pre-calculus lesion of the renal papilla in the 1930s and this was substantiated by others during the next decade and then largely ignored. This insignificant subepithelial calcification of the renal papilla. Randall's plaque type I, becomes the nucleus of at least 15% of calcium oxalate calculi, as demonstrated by apatite nuclei existing in papillary depression on the external stone surface. Cross section study of the stone demonstrates the peripheral nucleus with eccentric lamination postulating a mural origin. Contrariwise, study of the stone developing upon a nucleus originating in the papillary ducts (without producing obstruction) or out in the calix demonstrates a central nucleus surrounded by concentric laminations or lack of a mural origin, the more common type of calcium oxalate stone structure. Obstruction of the papillary ducts by hyperexcretion of stone salt may result in anemic infarction and sloughing of the apex of the papilla. Data concerning the prevalence of Randall's plaques in the population have been reviewed. Evidence of the incidence of calcium oxalate calculi that have developed upon Randall's plaques has been presented. A plea for further study of the pathology of the renal papilla has been voiced.

Topics: Calcium; Humans; Kidney Calculi; Oxalates; Ureteral Calculi

Topics: Calcium; Crystallization; Crystallography; Diet; Ethanol; Glycosaminoglycans; Humans; Kidney Calculi; Organophosphonates; Organophosphorus Compounds; Oxalates; Urinary Calculi

Topics: Calcium; Chemical Precipitation; Crystallization; Depression, Chemical; Diphosphates; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Pyrophosphatases; Recurrence; Time Factors

Topics: Adolescent; Adult; Aged; Ammonia; Calcium; Cystinuria; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Ureteral Obstruction; Uric Acid; Urinary Tract Infections

Topics: Child; Humans; Intestine, Small; Kidney Calculi; Liver Diseases; Malabsorption Syndromes; Oxalates

Topics: Cacao; Calcium, Dietary; Diet; Food Analysis; Humans; Ileum; Intestinal Absorption; Kidney Calculi; Oxalates; Tea; Vegetables

Topics: Calcium; Calcium Phosphates; Chemistry, Physical; Cystine; Hot Temperature; Humans; Kidney Calculi; Magnesium; Oxalates; Urea

Topics: Calcium; Humans; Kidney Calculi; Oxalates; Phosphates; Spectrophotometry, Infrared; Uric Acid; Xanthines

Topics: Animals; Citrates; Glyoxylates; Kidney Calculi; Malates; Oxalates; Oxaloacetates; Rats; Succinates; Succinimides

Topics: Adult; Bloodletting; Calcium; Creatinine; Female; Humans; Hypothermia, Induced; Ischemia; Kidney; Kidney Calculi; Kidney Pelvis; Male; Methods; Middle Aged; Oxalates; Perfusion; Phosphates; Quaternary Ammonium Compounds; Radiography; Renal Artery; Renal Veins; Suture Techniques; Temperature; Urea; Urine

Topics: Adult; Autopsy; Biopsy; Cadaver; Creatinine; Female; Humans; Kidney Calculi; Kidney Failure, Chronic; Kidney Transplantation; Metabolism, Inborn Errors; Oxalates; Renal Dialysis; Transplantation, Homologous

Topics: Acute Kidney Injury; Adult; Cadaver; Female; Fundus Oculi; Humans; Hydrochlorothiazide; Kidney Calculi; Kidney Cortex; Kidney Transplantation; Metabolism, Inborn Errors; Methylene Blue; Oxalates; Pyelonephritis; Pyridoxine; Transplantation, Homologous; Urinary Tract Infections

Topics: Calcium; Crystallization; Cystinuria; Diet Therapy; Humans; Kidney Calculi; Oxalates; Recurrence; Uric Acid; Urinary Tract Infections

Topics: Adult; Carbon Radioisotopes; Creatinine; Diet; Half-Life; Humans; Kidney; Kidney Calculi; Male; Metabolic Clearance Rate; Middle Aged; Oxalates; Probenecid

Topics: Bile; Calcium; Chemical Phenomena; Chemistry, Physical; Cholelithiasis; Cholesterol; Humans; Ions; Kidney Calculi; Oxalates; Phosphates; Solubility; Thiazines

Topics: Adult; Calcium; Cholestyramine Resin; Diarrhea; Diet; Diet Therapy; Diet, Reducing; Female; Humans; Intestine, Small; Kidney Calculi; Male; Middle Aged; Obesity; Oxalates; Postoperative Complications; Radiography; Taurine; Urinary Calculi

Topics: Adult; Age Factors; Aged; Body Weight; Calcium; Caseins; Creatinine; Glucose; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates

Topics: Administration, Oral; Adult; Calcium; Carbon Radioisotopes; Dietary Fats; Fatty Acids; Humans; Ileostomy; Ileum; Intestinal Absorption; Kidney Calculi; Malabsorption Syndromes; Middle Aged; Oxalates

Topics: Adult; Calcium; Glomerulonephritis; Humans; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Peritoneal Dialysis; Renal Dialysis

Topics: Adult; Calcium; Cholestyramine Resin; Diet Therapy; Humans; Ileum; Jejunum; Kidney Calculi; Male; Obesity; Oxalates; Postoperative Complications; Urography

Topics: Acids; Adult; Calcium; Citrates; Creatinine; Fasting; Fatty Acids, Nonesterified; Female; Glomerular Filtration Rate; Glucagon; Glucose Tolerance Test; Humans; Hyperparathyroidism; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Time Factors; Uric Acid

Topics: Adult; Age Factors; Carbon Radioisotopes; Child; Creatinine; Humans; Intestinal Absorption; Kidney Calculi; Kidney Concentrating Ability; Male; Middle Aged; Oxalates; Recurrence

Topics: Animals; Bile Acids and Salts; Carbon Isotopes; Cholelithiasis; Cholesterol; Diet; Feedback; Female; Haplorhini; Humans; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; Kidney Calculi; Lipid Metabolism; Liver; Male; Methods; Models, Biological; Oxalates; Phospholipids; Radioisotope Dilution Technique

Topics: Adolescent; Animals; Biopsy; Chick Embryo; Child; Child, Preschool; Humans; Infant; Kidney; Kidney Calculi; Kidney Diseases; Microscopy, Polarization; Nephrectomy; Oxalates; Tajikistan; Urinary Tract Infections

Topics: Apatites; Calcium; Calcium Phosphates; Cystine; Diphosphates; Gels; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Microscopy, Electron, Scanning; Models, Biological; Oxalates; Phosphates; Spectrophotometry, Infrared; Temperature; Uric Acid; X-Ray Diffraction; Xanthines

Topics: Humans; Kidney Calculi; Kidney Failure, Chronic; Oxalates

Topics: Amides; Animals; Diet; Female; Ischemia; Kidney; Kidney Calculi; Ligation; Male; Microscopy, Electron, Scanning; Nephrocalcinosis; Oxalates; Rabbits; Renal Artery; Renal Veins

Topics: Calcium; Humans; Kidney Calculi; Oxalates

Topics: Calcium; Cholelithiasis; Humans; Kidney Calculi; Liver Diseases; Oxalates; Tyramine

Topics: Adolescent; Adult; Calcium; Cellulose; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates

Topics: Adolescent; Adult; Calcium; Defecation; Female; Humans; Ileum; Jejunum; Kidney Calculi; Male; Michigan; Middle Aged; Obesity; Oxalates; Serum Albumin; Uric Acid; Urography

Topics: Humans; Ileum; Intestinal Diseases; Kidney Calculi; Metabolic Diseases; Oxalates; Taurine

Topics: Calcium; Chlorides; Citrates; Kidney Calculi; Magnesium; Oxalates; Sodium Chloride; Solubility

Topics: Adolescent; Adult; Aged; Biopsy; Calcium; Child; Child, Preschool; Colonic Neoplasms; Cystine; Epithelial Cells; Female; Humans; Hyperparathyroidism; Kidney Calculi; Kidney Tubules, Distal; Male; Middle Aged; Nephrocalcinosis; Nephrons; Oxalates; Peptic Ulcer; Phosphates; Uric Acid; Urinary Tract Infections

Topics: Humans; Kidney Calculi; Oxalates; Uric Acid

Topics: Adolescent; Adult; Calcium; Cellulose; Creatinine; Diet; Female; Humans; Hyperparathyroidism; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Phosphorus; Zinc

Topics: Alkaline Phosphatase; Calcium; Creatinine; Diet; Female; Follow-Up Studies; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Oxalates; Phosphates; Phosphorus; Pyridoxine; Radiography; Time Factors; Uric Acid

Topics: Apatites; Calcium; Chemical Phenomena; Chemistry, Physical; Cystine; Cystinuria; Female; Humans; Kidney Calculi; Male; Methods; Oxalates; Spectrophotometry, Infrared; Temperature; Uric Acid; X-Ray Diffraction

Topics: Binding Sites; Calcium; Crystallization; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Kinetics; Magnesium; Molecular Conformation; Oxalates; Particle Size; Spectrophotometry, Infrared; Water

Topics: Adult; Blood Urea Nitrogen; Bone and Bones; Cardiomyopathies; Female; Heart Block; Heart Conduction System; Heart Failure; Humans; Kidney; Kidney Calculi; Kidney Failure, Chronic; Metabolism, Inborn Errors; Myocardium; Nephrectomy; Oxalates; Pancreas; Renal Dialysis; Thyroid Gland

Topics: Adult; Humans; India; Kidney Calculi; Oxalates; Phosphates; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; X-Ray Diffraction

Topics: Amylases; Clinical Enzyme Tests; Enzymes; Humans; Kidney Calculi; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; Malate Dehydrogenase; Oxalates

Topics: Adolescent; Adult; Age Factors; Child; Child, Preschool; Female; Hematuria; Hospitalization; Humans; Infant; Iran; Kidney Calculi; Male; Oxalates; Rectal Prolapse; Sex Factors; Socioeconomic Factors; Ureteral Calculi; Urinary Bladder Calculi; Urinary Calculi

Topics: Adult; Bile Acids and Salts; Cholestyramine Resin; Diarrhea; Feces; Humans; Kidney Calculi; Male; Oxalates; Taurine; Tritium

Topics: Administration, Oral; Animals; Citrates; Citric Acid Cycle; Disease Models, Animal; Ethylene Glycols; Glyoxylates; Hydroxyproline; Injections, Intraperitoneal; Kidney Calculi; Malates; Oxalates; Oxaloacetates; Rats; Succinates

Topics: Adult; Autopsy; Cadaver; Creatinine; Graft Rejection; Humans; Immunosuppression Therapy; Kidney; Kidney Calculi; Kidney Transplantation; Male; Metabolism, Inborn Errors; Nephrectomy; Oxalates; Transplantation, Homologous

Topics: Calcium; Diet Therapy; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Oxalates; Phosphates; Solubility

Topics: Acute Disease; Animals; Chromatography, Gas; Citrates; Citric Acid Cycle; Drug Synergism; Glyoxylates; Injections, Intraperitoneal; Kidney Calculi; Male; Oxalates; Rats

Topics: Administration, Oral; Adult; Calcium; Crystallization; Diet; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence

Topics: Child; Diet Therapy; Female; Humans; Kidney Calculi; Oxalates; Urography

Topics: Calcium; Crystallization; Humans; Kidney Calculi; Oxalates; Water

Topics: Allopurinol; Child; Female; Glycolates; Glyoxylates; Humans; Isocarboxazid; Ketoglutaric Acids; Kidney Calculi; Metabolism, Inborn Errors; Muscles; Oxalates; Pyridoxine; Uric Acid

Topics: Calcium; Chromatography, Gas; Humans; Kidney Calculi; Oxalates; Uric Acid

Topics: Diet Therapy; Humans; Kidney Calculi; Male; Oxalates

Topics: Animals; Basement Membrane; Calcium; Diet; Kidney Calculi; Kidney Tubules; Magnesium; Male; Microscopy, Electron; Oxalates; Phosphorus; Pyridoxine; Rats; Rats, Inbred Strains; Sodium; Spectrum Analysis

Topics: Adult; Aged; Bile Acids and Salts; Cholestyramine Resin; Female; Humans; Ileum; Intestinal Diseases; Kidney Calculi; Male; Metabolic Diseases; Middle Aged; Oxalates; Urography

Topics: Bile Acids and Salts; Carbon Isotopes; Glycine; Glycolates; Humans; Ileum; Intestinal Diseases; Kidney Calculi; Metabolic Diseases; Oxalates

Topics: Diet; Female; Humans; Kidney Calculi; Male; Methods; Oxalates

Topics: Calcium; Chemistry Techniques, Analytical; Citrates; Female; Hippurates; Humans; Kidney Calculi; Lactates; Male; Oxalates; Sex Factors

Topics: Adolescent; Adult; Calcium; Creatinine; Humans; Kidney Calculi; Magnesium; Male; Microscopy, Electron; Middle Aged; Natriuresis; Oxalates; Paraplegia; Phosphates; Potassium; Quadriplegia; Spinal Cord Injuries

Topics: Calcium; Chromatography; Citrates; Creatinine; Culture Techniques; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Oxalates; Phosphates; Phosphorus; Urine

Topics: Adult; Calcium, Dietary; Creatinine; Diet; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates

Topics: Ascorbic Acid; Humans; Kidney Calculi; Oxalates

Topics: Animals; Apatites; Calcium; Calcium Carbonate; Crystallography; Horse Diseases; Horses; Kidney; Kidney Calculi; Male; Oxalates

Topics: Adult; Autopsy; Female; Humans; Intestine, Small; Kidney; Kidney Calculi; Lung; Metabolism, Inborn Errors; Myocardium; Oxalates; Pancreas; Parathyroid Glands; Pyelonephritis; Thyroid Gland; Trachea

Topics: Adult; Bicarbonates; Crystallography; Cystine; Cystinuria; Hematuria; Humans; Hydroxyapatites; Kidney Calculi; Male; Oxalates; Radiography; Water; X-Ray Diffraction

Topics: Acid-Base Equilibrium; Adult; Allopurinol; Ammonia; Blood Proteins; Calcium; Citrates; Creatinine; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Oxalates; Potassium; Sodium; Statistics as Topic; Uric Acid; Xanthine Oxidase

Topics: Adult; Calcium; Calcium Phosphates; Colorimetry; Electron Probe Microanalysis; Humans; Hydrogen-Ion Concentration; Hydroxyapatites; Kidney Calculi; Male; Middle Aged; Oxalates; Recurrence; Urine

Topics: Animals; Bacteria; Biological Transport, Active; Crystallization; Injections, Intraperitoneal; Intestinal Absorption; Kidney; Kidney Calculi; Lymphatic System; Microspheres; Oxalates; Polyvinyls; Pyelonephritis; Rats; Sulfonamides

Topics: Calcium; Diuretics; Female; Hematuria; Humans; Kidney Calculi; Kidney Pelvis; Male; Oxalates; Phosphates; Sex Factors; Uric Acid; Urinary Tract Infections; Vibration

Topics: Aged; Calcium, Dietary; Child; Diet; Dietary Fats; Dietary Proteins; Edible Grain; Feeding Behavior; Female; Food Analysis; Fruit; Humans; India; Kidney Calculi; Lactation; Oxalates; Plants, Edible; Pregnancy; Rural Population; Seasons; Socioeconomic Factors; Urban Population; Vegetables

Topics: Animal Nutritional Physiological Phenomena; Animals; Calcium; Crystallization; Food Deprivation; Glycine; Glycols; Glyoxylates; Kidney; Kidney Calculi; Male; Myocardium; Oxalates; Rats; Thiamine Deficiency; Time Factors; Vitamin B 6 Deficiency

Topics: Adult; Aged; Bacteria; Bile Acids and Salts; Calcium; Colon; Female; Glycine; Glyoxylates; Humans; Ileum; Intestinal Diseases; Kidney Calculi; Male; Middle Aged; Oxalates; Taurine

Topics: Animals; Calcium; Guinea Pigs; Hydroxyproline; Injections, Intraperitoneal; Kidney; Kidney Calculi; Mice; Oxalates; Rats

Topics: Administration, Oral; Animals; Blood Cell Count; Blood Glucose; Blood Urea Nitrogen; Dimethyl Sulfoxide; Glycols; Injections, Intramuscular; Kidney; Kidney Calculi; Organ Size; Oxalates; Rats

Topics: Adolescent; Adult; Amino Acid Metabolism, Inborn Errors; Child; Female; Glyoxylates; Humans; Kidney Calculi; Magnesium Oxide; Nephrocalcinosis; Oxalates; Recurrence

Topics: Adult; Cystine; Cystinuria; Diet Therapy; Female; Humans; Kidney Calculi; Oxalates; Pregnancy; Urography

Topics: Adult; Female; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphorus; Pyridoxine

Topics: Biotransformation; Fluorides; Humans; Kidney Calculi; Kidney Diseases; Methoxyflurane; Oxalates

Topics: Calcium; Crystallization; Hydrogen-Ion Concentration; Hydroxyapatites; Kidney Calculi; Oxalates; Phosphates

Topics: Adult; Calcium; Calcium Phosphates; Chelating Agents; Child; Crystallization; Humans; Kidney Calculi; Methylene Blue; Oxalates; X-Ray Diffraction

Topics: Adult; Aged; Calcium; Female; Humans; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates

Topics: Calcium; Chromatography, Thin Layer; Colorimetry; Humans; Kidney Calculi; Magnesium; Methods; Microchemistry; Oxalates; Oxidation-Reduction; Phosphates; Time Factors; Uric Acid

Topics: Adolescent; Adult; Calcium; Child; Female; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Pyrrolidinones; Succinimides; Time Factors; Urinary Calculi

Topics: Calcium; Humans; Kidney Calculi; Microscopy, Polarization; Oxalates; Phosphates; Pyelonephritis; Urinary Calculi

Topics: Adult; Calcium; Calcium Phosphates; Circadian Rhythm; Citrates; Female; Humans; Hydrogen-Ion Concentration; Hydroxyapatites; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Time Factors

Topics: Calcium Metabolism Disorders; Glycolates; Humans; Ileum; Intestinal Diseases; Kidney Calculi; Liver; Oxalates; Postoperative Complications; Recurrence; Taurine

Topics: Adult; Ammonia; Calcium; Calcium Phosphates; Diet; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Solubility; Spectrum Analysis; Uric Acid

Topics: Adult; Aged; Apatites; Calcium Phosphates; Cystine; Female; Humans; Hydroxyapatites; Kidney Calculi; Male; Middle Aged; Oxalates; Scotland; Sudan; United States; Uric Acid; Urinary Calculi; X-Ray Diffraction

Topics: Adult; Female; Humans; Kidney Calculi; Male; Oxalates

Topics: Acute Kidney Injury; Aged; Anuria; Calcium; Child; Female; Humans; Kidney Calculi; Kidney Tubules; Male; Methoxyflurane; Middle Aged; Oxalates; Postoperative Complications; Uremia

Topics: Adult; Aged; Aorta; Autopsy; Child; Female; Glycols; Humans; Kidney Calculi; Male; Metabolic Diseases; Myocardium; Nephrocalcinosis; Nephrosis; Oxalates; Pulmonary Alveoli; Spine; Spleen; Thyroid Gland

Topics: Calcium; Carbonates; Humans; Kidney Calculi; Kidney Pelvis; Magnesium; Oxalates; Phosphates; Quaternary Ammonium Compounds; Sex Factors; Ureteral Calculi; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; X-Ray Diffraction

Topics: Cystine; Diet Therapy; Humans; Kidney Calculi; Oxalates; Phosphates; Uric Acid

Topics: Ascorbic Acid; Aspirin; Asthma; Calcium; Citrates; Coronary Disease; Depression, Chemical; Diabetes Mellitus; Duodenal Ulcer; Dwarfism, Pituitary; Emphysema; Facial Paralysis; Gluconates; Histamine H1 Antagonists; Humans; Hypertension; Hyperthyroidism; Kidney Calculi; Liver Diseases, Parasitic; Magnesium; Oxalates; Phosphates; Pyridoxine; Schistosomiasis; Stimulation, Chemical; Terpenes; Tuberculosis, Pulmonary

Topics: Calcium; Female; Humans; Kidney Calculi; Male; Oxalates; Uric Acid; Yugoslavia

Topics: Animals; Body Weight; Calcium; Castration; Citrates; Female; Kidney Calculi; Liver; Magnesium; Male; Nutritional Requirements; Oxalates; Pyridoxine; Sex Factors; Time Factors; Ureteral Calculi; Urinary Bladder Calculi; Urinary Calculi; Vitamin B 6 Deficiency; Xanthurenates

Topics: Adult; Ammonium Chloride; Calcium; Child; Dialysis; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Male; Oxalates; Pyrophosphatases; Quaternary Ammonium Compounds; Sulfates; Urea

Topics: Allopurinol; Calcium; Creatinine; Cystinuria; Diuresis; Humans; Kidney; Kidney Calculi; Magnesium; Metabolic Diseases; Methylene Blue; Oxalates; Penicillamine; Phosphates; Uric Acid; Urinary Tract Infections; Urine; Water-Electrolyte Balance

Topics: Adult; Calcium; Humans; Kidney Calculi; Male; Oxalates; Solvents

Topics: Adult; Allopurinol; Humans; Kidney Calculi; Male; Middle Aged; Oxalates; Pedigree; Sex Factors; Uric Acid

Topics: Balneology; Female; France; Humans; Kidney Calculi; Male; Mineral Waters; Oxalates

Topics: Adult; Calcium; Humans; Kidney Calculi; Male; Oxalates

Topics: Adult; Calcium; Creatinine; Crystallization; Diet; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphates

Topics: Acetates; Amino Acids; Calcium; Calcium Isotopes; Chromatography, Gel; Citrates; Formates; Humans; Hypoparathyroidism; Kidney Calculi; Magnesium; Oxalates; Paget Disease, Extramammary; Phosphates; Protein Binding; Quaternary Ammonium Compounds; Sulfates

Topics: Animals; Calcium; Crystallography; History, 18th Century; Humans; Hypercalcemia; Kidney Calculi; Mice; Mitosis; Neoplasms, Experimental; Occupational Diseases; Oxalates; Phosphates; Sulfonamides; United Kingdom; Urinary Bladder; Urinary Bladder Neoplasms

Topics: Adolescent; Adult; Ammonium Chloride; Bicarbonates; Calcium; Calcium, Dietary; Circadian Rhythm; Diffusion; Edetic Acid; Ethinyl Estradiol; Fasting; Glutamates; Glycine; Humans; Hyperparathyroidism; Hypoparathyroidism; Kidney Calculi; Magnesium; Male; Oxalates; Purines

Topics: Aged; Calcium; Humans; Kidney Calculi; Male; Oxalates; Uric Acid; Urography

Topics: Hydroxyapatites; Infrared Rays; Kidney Calculi; Oxalates; Phosphates; Radiography; Uric Acid; X-Ray Diffraction

Topics: Calcium; Humans; Kidney Calculi; Mathematics; Methods; Oxalates; Phosphates; Solvents

Topics: Adult; Creatinine; Female; Humans; Kidney Calculi; Metabolic Diseases; Oxalates; Peritoneal Dialysis; Peritoneum; Permeability; Urea

Topics: Adult; Blood Vessels; Cardiomyopathies; Female; Heart Conduction System; Humans; Kidney Calculi; Male; Metabolic Diseases; Nephrocalcinosis; Oxalates; Pregnancy; Renal Dialysis

Topics: Citrates; Humans; Kidney Calculi; Oxalates; Temperature; Uric Acid

Topics: Calcium; Humans; Kidney Calculi; Microscopy, Polarization; Oxalates; Phosphates; Radiography; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aged; Calcium; Calcium, Dietary; Citrates; Female; Humans; Kidney Calculi; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Phosphorus; Recurrence; Time Factors; Urinary Tract Infections

Topics: Allopurinol; Calcium; Calcium Phosphates; Chemical Phenomena; Chemistry; Citrates; Cystine; Diagnosis, Differential; Diet Therapy; Humans; Kidney Calculi; Magnesium; Oxalates; Penicillamine; Phosphates; Quaternary Ammonium Compounds; Uric Acid; Xanthines

Topics: Animals; Crystallization; Humans; Kidney; Kidney Calculi; Male; Oxalates; Pyelonephritis; Rats

Topics: Calcium; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Osmolar Concentration; Oxalates; Phosphates; Potassium; Quaternary Ammonium Compounds; Sodium; Solubility; Sulfates

Topics: Ammonium Chloride; Animals; Bicarbonates; Calcium; Diet Therapy; Glycols; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Oxalates; Rats; Urinary Calculi; Vitamin B 6 Deficiency

Topics: Chemistry Techniques, Analytical; Cystine; Hot Temperature; Humans; Kidney Calculi; Magnesium; Methods; Oxalates; Phosphates; Quaternary Ammonium Compounds; Uranium

Topics: Calcium; Diet; Humans; Kidney Calculi; Male; Oxalates

Topics: Age Factors; Calcium; Colorimetry; Cystine; Diagnosis, Differential; Female; Hair; Humans; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Phosphorus; Photometry; Potassium; Sex Factors; Sodium; Statistics as Topic; Uric Acid

Topics: Adult; Animals; Calcium; Diet; Dietary Carbohydrates; Glomerular Filtration Rate; Glucose; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Magnesium; Male; Middle Aged; Milk; Oxalates; Sucrose

Topics: Adrenocorticotropic Hormone; Adult; Calcium; Colitis, Ulcerative; Crohn Disease; Female; Humans; Ileitis; Inflammation; Intestinal Diseases; Kidney Calculi; Male; Oxalates; Proctoscopy; Uric Acid; Urologic Diseases

X-ray diffraction studies have shown that there are several different kinds of human urinary calculi, with different age, sex, period, and geographical distributions. Juvenile bladder stones are typically urate and oxalate in small boys in certain stone belts. They have disappeared in some areas, particularly in Britain, but are still common in Thailand. India. and Turkey. Their cause is unknown. Adult bladder stones, formerly common in elderly men, were largely of uric acid and were due to a faulty diet. Juvenile kidney stones are rare, except in Turkey where they are similar to juvenile bladder stones. Adult kidney stones are by far the most universally common, especially in technically developed communities. They are found in both sexes (equally at postmortem), and in the United States and in Czechoslovakia the average number of hospital entries for stones, relative to the whole population, is about 1 per 1000 per annum (increasing) although the incidence in different districts varies by 4 to 1 or more. Such stones are mainly calcium oxalates and calcium and MgNH(4) phosphates. The incidence among the administrative class is at least 20 times that among agricultural workers, relative to their numbers. Stones are reported also to be an occupational hazard for air pilots. It is probably that much more exercise and the drinking of more water to prevent kidney dehydration (spirits and coffee are not effective for this purpose) would lower the high rate of incidence. Moderate acidification would prevent phosphate supersaturation of the urine, but is not effective for oxalates. It seems certain that, once a suitable seed is formed, epitaxy is largely responsible for deposition from urines that would otherwise remain supersaturated until voided. This would explain the curioLls radial and layered texture of many stones. Laboratory experiments might suggest ways of preventing orientated overgrowth.

Topics: Calcium Phosphates; Calculi; Crystallization; Czechoslovakia; History, 18th Century; History, 19th Century; History, 20th Century; Humans; India; Italy; Kidney Calculi; Occupational Diseases; Oxalates; Spain; Thailand; Turkey; United Kingdom; Ureteral Calculi; Ureteral Obstruction; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; X-Ray Diffraction; Zimbabwe

Topics: Adult; Alcohol Oxidoreductases; Carbon Isotopes; Child; Child, Preschool; Clinical Enzyme Tests; Diagnosis, Differential; Female; Glyceric Acids; Glycolates; Glyoxylates; Humans; Kidney Calculi; Ligases; Male; Metabolism, Inborn Errors; Oxalates; Pyruvates

Topics: Adult; Calcium; Child; Child, Preschool; Female; Glyoxylates; Humans; Kidney; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates

Topics: Adult; Child; Chromatography; Colorimetry; Female; Glyceric Acids; Humans; Kidney Calculi; Male; Metabolism, Inborn Errors; Methods; Nephrocalcinosis; Optical Rotatory Dispersion; Oxalates

Topics: Age Factors; Calcium; Genes, Dominant; Genes, Recessive; Humans; Kidney Calculi; Oxalates; Sex Factors; Urinary Tract Infections

Topics: Chemistry Techniques, Analytical; Cholesterol; Fucose; Galactose; Glucose; Hexosamines; Hexoses; Humans; In Vitro Techniques; Kidney Calculi; Mannose; Mucoproteins; Neuraminic Acids; Oxalates; Proteins; Uric Acid

Topics: Ammonia; Amylases; Calcium; Chemistry Techniques, Analytical; Enzyme Induction; Humans; Hyaluronoglucosaminidase; In Vitro Techniques; Kidney Calculi; Mucoproteins; Muramidase; Oxalates; Pancreatic Elastase; Papain; Phosphates; Proteins; Trypsin

Topics: Adult; Africa; Asia; Calcium; Child; Diet; Humans; Kidney Calculi; Oxalates; Racial Groups; United Kingdom; United States; Urinary Bladder Calculi; Urinary Calculi

Topics: Adult; Calcium; Humans; Kidney Calculi; Magnesium; Oxalates; Prognosis

Topics: Acidosis, Renal Tubular; Calcium; Female; Humans; Hyperparathyroidism; Ions; Kidney Calculi; Magnesium; Male; Oxalates; Phosphates; Quaternary Ammonium Compounds; Solubility; Urinary Tract Infections

Topics: Adult; Age Factors; Aged; Body Height; Body Weight; Czechoslovakia; Factor Analysis, Statistical; Female; Humans; Kidney Calculi; Male; Middle Aged; Obesity; Oxalates; Phosphates; Sex Factors; Uric Acid

Topics: Adolescent; Adult; Age Factors; Aged; Apatites; Calcium Phosphates; Child; Child, Preschool; Cystine; Czechoslovakia; England; Female; Humans; Hydroxyapatites; India; Indonesia; Infant; Kidney Calculi; Male; Middle Aged; Minerals; Oxalates; Sex Factors; Spain; Thailand; Turkey; Ureteral Calculi; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; X-Ray Diffraction

Topics: Adult; Calcium; Crystallography; Humans; Kidney Calculi; Kidney Tubules; Male; Metabolism, Inborn Errors; Microscopy, Electron; Nephrectomy; Oxalates

Topics: Calcium; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Uric Acid; Urinary Calculi

Topics: Adult; Female; Hair; Humans; Intestinal Absorption; Kidney Calculi; Magnesium; Male; Oxalates

Topics: Adolescent; Adult; Allopurinol; Child; Child, Preschool; Female; Humans; Kidney Calculi; Male; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates

Topics: Humans; Kidney Calculi; Magnesium Oxide; Oxalates; Pyridoxine

Topics: Acid-Base Equilibrium; Gout; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Oxalates; Urinary Bladder Calculi

Topics: Acidosis, Renal Tubular; Alcohol Oxidoreductases; Allopurinol; Biopsy; Blood Urea Nitrogen; Calcium Metabolism Disorders; Disulfiram; Enzyme Repression; Glyoxylates; Humans; Kidney; Kidney Calculi; Kidney Failure, Chronic; Leukocytes; Nephrocalcinosis; Oxalates; Pyridoxine

Topics: Adult; Aged; Ammonia; Autoanalysis; Humans; Hydrogen-Ion Concentration; Kidney Calculi; Middle Aged; Oxalates; Uric Acid; Urine

Topics: Calcium; Female; Follow-Up Studies; Humans; Kidney Calculi; Magnesium Oxide; Male; Oxalates; Pyridoxine

Topics: Adolescent; Child; Female; Humans; Kidney; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Radiography

Topics: Adolescent; Adult; Alanine; Child; Child, Preschool; Female; Glomerulonephritis; Glutamates; Glycine; Glycolates; Glyoxylates; Humans; In Vitro Techniques; Kidney Calculi; Male; Oxalates; Transaminases; Vitamin B 6 Deficiency

Topics: Humans; Kidney Calculi; Oxalates

Topics: Adolescent; Axilla; Calcinosis; Humans; Kidney Calculi; Male; Oxalates; Skin Diseases; Thigh

Topics: Calcium; Humans; Kidney Calculi; Magnesium; Oxalates; Phosphorus; Pyridoxine

Topics: Calcium; Female; Humans; Kidney Calculi; Middle Aged; Oxalates

Topics: Adrenal Cortex Hormones; Adult; Calcium; Diagnosis, Differential; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Liver Diseases; Lung Diseases; Male; Oxalates; Radiography; Sarcoidosis

Topics: Calcium; Humans; Hungary; Kidney Calculi; Magnesium; Magnesium Deficiency; Oxalates; Phosphates; Water Supply

Topics: Calcium; Calcium Carbonate; Chemistry Techniques, Analytical; Chemistry, Clinical; Hot Temperature; Humans; Kidney Calculi; Methods; Oxalates; Uric Acid

Topics: Adolescent; Adult; Animals; Diuretics; Female; Humans; Kidney Calculi; Male; Mice; Middle Aged; Oxalates; Plant Extracts; Plants; Radiography; Ureteral Calculi

Topics: Adult; Cardiomegaly; Humans; Kidney Calculi; Male; Metabolism, Inborn Errors; Myocarditis; Nephritis, Interstitial; Oxalates; Radiology

Topics: Calcium; Calcium Phosphates; Chemistry Techniques, Analytical; Humans; Kidney Calculi; Male; Oxalates; Urine

Topics: Adult; Female; Humans; Kidney Calculi; Metabolic Diseases; Nephrocalcinosis; Oxalates

Topics: Female; Genetics, Medical; Humans; Kidney Calculi; Male; Oxalates; Phosphates; Sex; Uric Acid

Topics: Animals; Calcium; Diet Therapy; Foreign Bodies; Kidney Calculi; Magnesium; Oxalates; Rats; Urinary Bladder Calculi; Vitamin B 6 Deficiency

Topics: Amides; Animals; Cricetinae; Dogs; Guinea Pigs; Kidney Calculi; Oxalates; Rabbits; Rats; Swine

Topics: Animals; Cricetinae; Crystallization; Guinea Pigs; Humans; Kidney Calculi; Oxalates; Rabbits; Urinary Calculi

Topics: Humans; Kidney Calculi; Oxalates; Ureteral Calculi; Uric Acid

Topics: Blood; Body Fluids; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Nephrolithiasis; Oxalates; Uric Acid; Urine

Two patients, aged 66 and 62 years, are described who suffered from unilateral anuria and contralateral stone formation due to primary oxalosis. The diagnosis was established by microscopical examination of necropsy material in the first patient and by renal biopsy in the second and was confirmed by chemical and x-ray investigation of tissues and calculi. The sequence of events leading to the rather sudden precipitation of oxalate in the tissues is discussed, and a tentative explanation for the unilateral anuria is offered.

Topics: Aged; Anuria; Biopsy; Geriatrics; Humans; Hyperoxaluria, Primary; Kidney Calculi; Kidney Glomerulus; Microscopy; Nephrectomy; Oxalates; Pathology

Topics: Consanguinity; Heart Block; Humans; Hyperoxaluria; Kidney Calculi; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates; Pancreatitis; Pathology; Skin Diseases; Uremia; Urine

Topics: Humans; Hyperoxaluria, Primary; Kidney Calculi; Metabolism, Inborn Errors; Oxalates

Topics: Alkaline Phosphatase; Ammonium Compounds; Calcium Phosphates; Cystine; Fluorescence; Fluorescent Antibody Technique; Histocytochemistry; Humans; Kidney; Kidney Calculi; Kidney Tubules; Microscopy; Microscopy, Fluorescence; Mucoproteins; Oxalates; Pathology; Phosphates; Quaternary Ammonium Compounds; Research; Uric Acid; Uromodulin

Topics: Alkaline Phosphatase; Ammonium Compounds; Calcium Phosphates; Cystine; Fluorescence; Fluorescent Antibody Technique; Histocytochemistry; Humans; Kidney; Kidney Calculi; Microscopy; Microscopy, Fluorescence; Mucoproteins; Oxalates; Pathology; Phosphates; Quaternary Ammonium Compounds; Research; Uric Acid

Topics: Adolescent; Amino Acid Metabolism, Inborn Errors; Carbon Isotopes; Family; Glycine; Glycolates; Glyoxylates; Hippurates; Humans; Hydroxyproline; Kidney Calculi; Nephrocalcinosis; Oxalates; Urine

Topics: Acidosis, Renal Tubular; Adolescent; Adult; Aged; Calcium; Child; Female; Humans; Hyperparathyroidism; Kidney Calculi; Male; Middle Aged; Oxalates; Phosphorus; Urinary Calculi

Topics: Adult; Child; Humans; In Vitro Techniques; Kidney Calculi; Male; Oxalates; Urine

Topics: Adult; Biopsy; Humans; Kidney Calculi; Male; Metabolism, Inborn Errors; Oxalates; Urinary Calculi

Topics: Asia, Western; Chemistry Techniques, Analytical; Crystallography, X-Ray; Ethnology; Humans; Kidney Calculi; Oxalates; Surgical Procedures, Operative; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; X-Ray Diffraction

Topics: Administration, Oral; Body Fluids; Calcium; Calcium, Dietary; Humans; Kidney Calculi; Magnesium; Metabolism; Oxalates; Phosphates; Urine

Topics: Citrates; Humans; Kidney Calculi; Lithiasis; Nephritis; Nephrolithiasis; Oxalates; Phosphates; Uric Acid; Urine

Topics: Anemia; Anemia, Hypochromic; Anuria; Hematologic Diseases; Humans; Hyperoxaluria; Kidney Calculi; Oxalates; Toxicology

Topics: Crystallization; Electrons; Hyperoxaluria; Injections, Intraperitoneal; Kidney; Kidney Calculi; Microscopy; Microscopy, Electron; Oxalates; Pharmacology; Rats; Research; X-Rays

Topics: Amino Acid Metabolism, Inborn Errors; Calcinosis; Glycine; Glycolates; Humans; Hyperoxaluria, Primary; Kidney Calculi; Kidney Diseases; Oxalates; Transaminases; Urine; Vitamin B 6 Deficiency

Topics: Humans; Hyperoxaluria; Kidney Calculi; Oxalates

Topics: Benzoates; Child; Diet; Diet Therapy; Genetics, Medical; Humans; Hyperoxaluria, Primary; Kidney Calculi; Metabolic Diseases; Nephrocalcinosis; Oxalates; Surgical Procedures, Operative; Urine; Urography

Topics: Body Fluids; Glyoxylates; Humans; Hyperoxaluria, Primary; Keto Acids; Kidney Calculi; Metabolic Diseases; Nephrocalcinosis; Oxalates; Urine

Topics: Calcium; Calcium, Dietary; Citrates; Kidney Calculi; Magnesium; Nephrolithiasis; Oxalates; Pharmacology; Phosphates; Phosphorus; Phosphorus, Dietary; Pyridoxine; Rats; Research; Sulfates; Sulfur; Urine; Vitamin B 6

Topics: Biochemical Phenomena; Biochemistry; Calcium Metabolism Disorders; Humans; Hyperparathyroidism; Kidney Calculi; Lithiasis; Metabolism; Oxalates; Uric Acid

Topics: Humans; Kidney Calculi; Lithiasis; Nephrolithiasis; Oxalates; Phosphates; Psychophysiologic Disorders; Psychosomatic Medicine; Psychotherapy; Research; Uric Acid

Topics: Acidosis; Alkalies; Humans; Hyperparathyroidism; Kidney Calculi; Lithiasis; Milk; Nephrolithiasis; Osteoporosis; Oxalates; Sarcoidosis; Urinary Tract Infections; Vitamin D

Topics: Antibodies; Calcium Compounds; Humans; Kidney Calculi; Oxalates; Oxides; Phosphates; Urinary Calculi

Topics: Acute Kidney Injury; Child; Humans; Hyperoxaluria; Infant; Kidney Calculi; Nephrolithiasis; Oxalates; Renal Insufficiency; Urinary Calculi

Topics: Calcium; Disease; Humans; Kidney Calculi; Oxalates; Parathyroid Diseases; Parathyroid Glands; Phosphates; Urinary Calculi

Topics: Calculi; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney; Kidney Calculi; Oxalates

Topics: Animals; Calculi; Cats; Kidney; Kidney Calculi; Nephrocalcinosis; Oxalates; Vitamin B 6 Deficiency; Vitamin B Deficiency; Vitamins

Topics: Body Fluids; Calculi; Humans; Kidney; Kidney Calculi; Nephrolithiasis; Oxalates; Oxalic Acid

Topics: Calcium Oxalate; Calculi; Humans; Kidney; Kidney Calculi; Oxalates; Urinalysis

Topics: Calculi; Humans; Kidney; Kidney Calculi; Oxalates

Topics: Calculi; Hyperoxaluria; Kidney; Kidney Calculi; Oxalates

Topics: Calcium Oxalate; Calculi; Humans; Kidney; Kidney Calculi; Nephrocalcinosis; Nephrolithiasis; Oxalates

Topics: Calcium; Calculi; Humans; Hyperoxaluria; Kidney; Kidney Calculi; Oxalates; Ureter